Monthly Archives: December 2014

Emergency Department Care Reconsidered


By Jeffrey E. Phillips BS, RN

What is patient care in the emergency department (ED) supposed to be about? Patients arrive either presenting with an already concluded diagnosis (e.g., “I cut my finger”, “I fell”) and require treatment, or a patient arrives with a set of symptoms that must have a diagnosis assigned to them (e.g., headache, chest pain, abdominal pain). In either possibility, the staff must determine the severity of the complaint, decide on a mode a treatment, and then transition the patient to treatment outside of the ED. That transition may be in the form of admission to the hospital, transfer to another facility, or discharge with or without primary care follow-up. Or in the words of emergency medicine physician, Dr. Ken Milne, “meet ‘em, greet ‘em, treat ‘em, and street ‘em” (Milne, 2014).

Our responsibility to our patients in the ED is about early intervention, stabilization, treatment, and transition, although according to Dr. Scott Weingart of Stony Brook University Hospital, it is much more than that. “Bring upstairs care, downstairs,” is the mantra Weingart tries to impart on those who will listen (Weingart, 2009). In a more verbose translation, he is advocating that the depth of care provided in the Intensive Care Unit (ICU) be provided in the ED as well. Of course Weingart is referring to the sickest of patients, those requiring the most intensive resuscitation efforts. But what about those patients outside of the resuscitation rooms; the rule out septicemia, the decompensated nursing home transfer, the undifferentiated abdominal pain? The concept of providing ICU or “floor” level care can be expanded to any patient in the ED. In the same way, the concept of providing excellent care goes beyond medicine and into nursing as well, or at least in theory it should.

As a gross generalization, emergency care boils down to treating emergent complaints and supporting airway, breathing and circulation (ABC) until the patient can be transferred to a facility or unit that is capable of more appropriately handling the patient’s condition. But in the modern, urban emergency department, overcrowding, long admission wait lists, and unsanitary conditions dampen what should be a seamless extension of excellent hospital care. The increase in patient visits coupled with the extended stays in the ED, both demand improved nursing care and also reduce the ability to provide it. As the patient census rises, and nurse-to-patient ratios creep into the teens, the ability to provide comprehensive care steadily diminishes. A patient load of twelve or fifteen patients devolves nursing care to the bare necessities of ensuring safety, monitoring ABCs, and providing “essential” treatment at the expense of quality patient-centered care.

emergency room     The implications of Dr. Weingart’s philosophy on medical practice is a conversation for another day. Discussions about whether to perform needle or knife cricothyrotomy, or when to implement extracorporeal membrane oxygenation on post-cardiac arrests patients is best left for medical experts to debate. The question posed here is whether Dr. Weingart’s philosophy of bringing floor level medical care in the ED can be extended to nursing care. Can nursing care bo optimize so that nurses go beyond efficiently keeping patient’s vitals stable and inserting IVs and Foley’s in the ED.

Something must change in this era when it is not unusual for 40% of patients in ED to be admitted, when the average wait time for an in-patient bed might take over 24 hours. It is interesting to consider how ED nurses perceive the level of care provided to “admitted” patients in the ED, those who are in transition limbo, praying for a bed (note to nursing students: this is an excellent researchable PICO project!). It is ironic that patients could be horizontal in the ED, but waiting for a bed. They are “resting” but yet there is something restless about and around them. How is the care different to the same type of patient, but one is “waiting” in the ED and the other is “waited on” in the medical-surgical unit? How do nurses make the distinction?

To illustrate this, let’s consider a scenario. Say an ED nurse is walking along a crowded corridor and saw an adult patient, tucked away in a corner stretcher, crying. The nurse recognized the patient as “not one of my patients”. Will the nurse go in and find out what’s happening with this patient. Or will the nurse simply walk on by and brush off the scene as “not an emergency” and move on perform another task? The incomplete explanation on what influences a nurse’s response to potential nursing moment in any setting is personal values. Every nurse agrees that nursing is the skilled (crafty in the positive sense) application of healing sciences, but ultimately it is also an attitude and a reflection of what the nurse holds true in his or her heart.

To fully integrate the ongoing ED initiatives to improve patient experience such as hourly rounding, reducing falls, decreasing incidence of left-without-being-seen, and providing timely antibiotic or discharge instructions requires a reflective recalibration of the collective and individual attitude of ED nurses or all nurses for that matter. It is troubling to note that medical records contain a disclaimer when a nursing procedure was performed in the ED (e.g., Foley insertion) as if it is probable that sterility may have been compromised. Floor level or ICU level nursing in the ED cannot be achieved by drive-by in-service but through careful consideration of personal values, mentorship and coaching, the use of checklists, and purposeful huddle to truly put patients first.

Increasing number of sicker patients will continue to descend upon the doors of EDs. In 2010, the number of visits to the ED increased by 32% nationwide, from 102.8 in 1999 to 129.8 million (Centers for Disease Control and Prevention, 2010). ED nurses, being the first nursing care contact of patients, will continue to rise to the challenge of implementing the same nursing care benchmarks for inpatients and leave a lasting positive impression in the patient beyond triage. Nurses save lives not just by cardiac compressions, but also holding our patients’ hands. In this regard, we are all floor nurses, no matter where we work.



Centers for Disease Prevention and Control. (2010). National Hospital Ambulatory Medical Care Survey: 2010 Emergency Department Summary Tables. Retrieved from

Milne, Ken MD (2014, Nov 16). The Skeptics Guide to Emergency Medicine (Audio Podcast). Retrieved from

Weingart, Scott MD. (2009, Mar 1). Emcrit Podcast (Audio Podcast). Retrieved from


Jeffrey PhillipsJeffrey E. Phillips BS, RN works in the Emergency Department at New York-Presbyterian Weil-Cornell Medical Center. Disclaimer: The views expressed in this essay are my own opinion and personal observations of patient care.

Propofol infusion syndrome: A rare but lethal complication

BY: Chen, Leon MS, RN, AGACNP-BC, CCRN, CPEN; Lim, Fidelindo A. DNP, RN, CCRN

MR. A, 48, WAS DIAGNOSED with diffuse large B-cell lymphoma and central nervous system involvement. Despite several rounds of chemotherapy and stem cell transplantation, his clinical status deteriorated. When video electroencephalography monitoring demonstrated refractory status epilepticus (RSE), he was transferred to the neurology observation unit of an urban cancer facility. RSE is defined as ongoing seizures following first- and second-line antiepileptic drug (AED) therapy.1

Mr. A required endotracheal intubation and mechanical ventilation. Despite multiple AEDs, including benzodiazepines, fosphenytoin, phenobarbital, valproic acid, and levetiracetam, he required a propofol infusion for subclinical seizure activity (no clinical or outward manifestation of the electrical seizure activity).2Burst suppression is a state of depressed brain activity achieved with anesthetics that’s used to combat status epilepticus.3 It wasn’t achieved despite a propofol infusion at 6 mg/kg/hr for more than 96 hours. Mr. A then developed a sudden onset of severe metabolic acidosis (serum lactic acid, 7 mmol/L [normal, less than 2 mmol/L]), profound refractory bradycardia, and hypotension (systolic BP less than 90 mm Hg) requiring vasopressors. Because he was hemodynamically unstable, he was transferred to the ICU.

In the ICU, Mr. A was found to have severe metabolic acidosis (pH 7.13) and rhabdomyolysis (creatine kinase 18,453 U/L [normal in males, 38-174 U/L]). His lactic acid level increased to 10.3 mmol/L. Mr. A’s blood specimens were repeatedly corrupted by severe lipemia. For this reason, his potassium level couldn’t be accurately measured. The combination of rhabdomyolysis (muscle tissue breakdown), dysrhythmia, cardiovascular failure, metabolic acidosis, and lab results strongly suggested propofol infusion syndrome (PRIS).

What’s known about PRIS?

An uncommon but potentially deadly complication of prolonged or high-dose propofol infusion, as well as high-dose short-term propofol infusions, PRIS is characterized by metabolic acidosis, hyperlipidemia, and cardiovascular collapse.4,5 Propofol is an ultra-short-acting I.V. sedative-hypnotic agent used primarily for the induction and maintenance of anesthesia or sedation for various indications, including reduction of intracranial pressure and burst suppression for RSE.6 Its rapid onset and elimination allow for quick weaning and neurologic assessments.7

Its anesthetic properties are thought to stem from its inhibition of the gamma-aminobutyric acid receptor, which also makes it effective for seizure suppression.7

In a large prospective study conducted in 2008, 1,017 patients from 11 ICUs who were suspected of having PRIS were observed. The inclusion criteria for PRIS were continuous propofol infusion followed by development of metabolic acidosis and cardiac dysrhythmia with the addition of rhabdomyolysis, hypertriglyceridemia, or renal failure.8 The syndrome was strongly associated with vasopressor use, probably because both propofol and catecholamines can cause muscle necrosis.9 It occurred most frequently after 48 to 72 hours of infusion. In this study, only a small percentage of PRIS cases were associated with a high propofol dose (greater than 4 mg/kg/hr); a dose-dependent relationship has been described in other studies.9

Case reports have described PRIS in patients undergoing burst suppression for RSE who received a high-dose propofol infusion or a large cumulative dose.10 Mr. A was strongly suspected of having developed PRIS while being treated with high-dose propofol for RSE. His rhabdomyolysis, metabolic acidosis, hypoxia, lipemia, and profound bradycardia unattributed to other causes fit the profile for PRIS.


Although the exact mechanism of PRIS isn’t well understood, it may be due to propofol’s disruption of the oxidative pathway in the mitochondria, leading to inhibition of adenosine triphosphate production in muscle tissues.11 This in turn causes diffuse cellular hypoxia and muscle necrosis.12 The muscle necrosis is further exacerbated by the catecholamine surge or increased vasopressor requirement secondary to cardiac depression resulting from propofol infusion.11

PRIS is considered a pharmacogenetic phenomenon, suggesting that some patients may have a specific susceptibility to the disease.13 A mitochondrial defect may predispose some patients to PRIS.14

Diagnostic criteria

Current diagnostic criteria include rhabdomyolysis, hyperkalemia, hyperlipidemia, renal failure, and Brugada-like electrocardiographic abnormalities, which includes ST-segment elevation (2 mm or greater) in leads V1 to V3 with the elevated ST segment descending with an upward convexity to an inverted T wave. This is referred to as the “coved type” Brugada pattern.12,15 Lipemia and elevated triglyceride levels have been documented in PRIS and may be the result of enhanced sympathetic nervous system stimulation and increased lipolysis.11 Additionally, propofol’s lipid emulsion is thought to cause accumulation of free fatty acids, leading to dysrhythmia.12 The patient shouldn’t have any known cause of heart failure or evidence of sepsis or multiorgan failure.

Currently, no standardized PRIS screening tool has been developed. A screening protocol based on creatine kinase and lactic acid levels has been studied in a single-center trial, but external validity hasn’t been established.11 The lack of a standardized screening tool for PRIS presents a challenge because many of the presenting signs (such as metabolic acidosis) are common in critically ill patients or are adverse reactions to propofol, such as bradycardia.9 Mr. A’s risk factors for PRIS are young age, RSE, I.V. vasopressor administration, high-dose propofol, and 96 hours of therapy.11

Nursing implications

In patients receiving I.V. propofol who have risk factors, including high doses (more than 4 mg/kg/hr), prolonged use (longer than 48 hr), critical illness, concomitant use of vasopressors or steroids, low carbohydrate intake, and relatively young age (less than age 55), hold a high index of suspicion of PRIS.11

Interdisciplinary collaboration among nurses, healthcare providers, and pharmacists is essential for the prompt recognition and treatment of PRIS. As part of surveillance for PRIS, critical care nurses should closely monitor arterial blood gas analysis results and serum metabolic profile, lactic acid, triglyceride, and creatine kinase levels, as well as liver profile and renal function study results. Nurses should also monitor results of ECGs and promptly report any episodes of hemodynamic instability.

Once signs and symptoms are recognized, immediately discontinue the propofol infusion and notify the healthcare provider. Though successful resuscitation with extracorporeal membrane oxygenation has been described in a case report,7 currently there are no definitive treatment guidelines apart from prompt discontinuation of propofol and supportive care.

In the ICU, Mr. A received supportive management that included fluid resuscitation, bicarbonate infusion, vasopressors, and serial monitoring of lab work. He was maintained on mechanical ventilation, his vital signs and urine output were closely monitored, and hourly neurologic assessments were performed.

Fatal outcome

Due to the heterogeneity of study criteria, illness presentation, and patient population studied, actual incidence and mortality of PRIS aren’t known. However, in spite of low estimated incidence rate (1%), the reported mortality ranges from 18% to over 50%.11

In this case, the propofol infusion was discontinued immediately once PRIS was suspected. Mr. A continued to receive benzodiazepines with close monitoring of hemodynamics. Unfortunately, despite optimal supportive care in the ICU, Mr. A experienced cardiac arrest and was unable to be successfully resuscitated.


Because no antidote for propofol exists, prevention is particularly crucial. An algorithm for preventing PRIS has been proposed but hasn’t been studied in clinical trials.16 Besides using alternative methods of sedation,9 preventive measures include infusing the lowest dose of propofol for the shortest duration, minimizing lipid load (concentrating propofol drip and adjusting parenteral nutrition), providing adequate carbohydrate intake, and stopping the propofol infusion at the earliest signs of abnormal lab results and/or ECG changes.10,11

Critical care nurses play a major role in early detection and prevention of PRIS by actively collaborating with healthcare providers during bedside rounds and periodic safety huddles during the course of treatment. Nurses can take leadership roles in designing quality improvement projects to prevent PRIS through shared governance committees. Evidence-based screening tools and definitive diagnostic guidelines need to be developed and implemented to improve patient outcomes.



1. Stecker MM. Status epilepticus. UpToDate. 2014.
2. Wilfong A. Overview of the classification, etiology, and clinical features of pediatric seizures and epilepsy. UpToDate. 2014.
3. Amzica F. Basic physiology of burst-suppression. Epilepsia. 2009; 50:(suppl 12):38–39.
4. Hwang WS, Gwak HM, Seo DW. Propofol infusion syndrome in refractory status epilepticus. J Epilepsy Res. 2013; 3:(1):21–27.
5. Tietze KJ, Fuchs B. Sedative-analgesic medications in critically ill adults: properties, dosage regimens, and adverse effects. UpToDate. 2014.
6. Propofol Injectable Emulsion [package insert]. Hospira, Inc., Lake Forest, IL; 2009.
7. Mayette M, Gonda J, Hsu JL, Mihm FG. Propofol infusion syndrome resuscitation with extracorporeal life support: a case report and review of the literature. Ann Intensive Care. 2013; 3:(1):32.
8. Roberts RJ, Barletta JF, Fong JJ, et al. Incidence of propofol-related infusion syndrome in critically ill adults: a prospective, multicenter study. Crit Care. 2009; 13:(5):R169
9. Imam TH. Propofol-related infusion syndrome: role of propofol in medical complications of sedated critical care patients. Perm J. 2013; 17:(2):85–87.
10. Iyer VN, Hoel R, Rabinstein AA. Propofol infusion syndrome in patients with refractory status epilepticus: an 11-year clinical experience. Crit Care Med. 2009; 37:(12):3024–3030.
11. Schroeppel TJ, Fabian TC, Clement LP, et al. Propofol infusion syndrome: a lethal condition in critically injured patients eliminated by a simple screening protocol. Injury. 2014; 45:(1):245–249.
12. Cremer OL. The propofol infusion syndrome: more puzzling evidence on a complex and poorly characterized disorder. Crit Care. 2009; 13:(6):1012
13. Annen E, Girard T, Urwyler A. Rare, potentially fatal, poorly understood propofol infusion syndrome. Clin Pract. 2012; 2:(3):e79
14. Savard M, Dupré N, Turgeon AF, Desbiens R, Langevin S, Brunet D. Propofol-related infusion syndrome heralding a mitochondrial disease: case report. Neurology. 2013; 81:(8):770–771.
15. Wylie JV, Garlitski AC. Brugada syndrome. UpToDate. 2014.
16. Testerman GM, Chow TT, Easparam S 4th.. Propofol infusion syndrome: an algorithm for prevention. Am Surg. 2011; 77:(12):1714–1715.

A full text version of this article can be found on the Nursing 2014 website at:

Leon ChenLeon Chen, MSc, AGACNP-BC, CCRN, CPEN
Leon Chen is Critical Care Medicine Nurse Practitioner of the Department of Anesthesiology and Critical Care Medicine at Memorial Sloan Kettering Cancer Center. He also serves as Adjunct Clinical Faculty for NYU College of Nursing and is a graduate of NYUCN’s bachelors and masters programs.



Fidel Lim Photo (2)

Fidelindo Lim, DNP, CCRN

Fidelindo Lim is a clinical faculty at NYU College of Nursing and a per diem nurse educator for NYP Weill Cornell and Hospital for Special Surgery.