practice updates

Recent updates and pitfalls in the emergency department evaluation and management of the septic joint.

From the understanding of physostigmine’s mechanism of action and the above data, we would like to summarize key points and recommendations regarding the use of physostigmine.

“I’ve got a pulse,” you hear the nurse shout. Finally, a sigh of relief comes over the crowded resuscitation room and you take a moment to reflect on what just happened… but, your work is just now about to truly begin. It is up to you to determine why the patient died in the first place and determine which crucial steps need to be initiated to increase your patient’s chance of survival.

Author: Zach Radwine, MD (EM Resident Physician, University of Illinois College of Medicine – Peoria) // Editors: Jennifer Robertson, MD, Lewis Nelson, MD and Alex Koyfman, MD (@EMHighAK) Featured on the LITFL Review #180 – Thanks to Joe-Anthony Rotella and the LITFL Review group for the shout out!  Introduction Carbon monoxide (CO) poisoning leads to an estimated 50,000 ED visits per year in the US.1 It is also the leading cause of death by poisoning.2,3,4,5 CO causes toxicity via binding with hemoglobin to form carboxyhemoglobin (COHb).  This reduces the oxygen carrying capacity of blood because hemoglobin binds CO with 210 times greater affinity than does O2.4,6 In addition CO produces toxicity by direct cellular damage by numerous mechanisms, including lipid peroxidation, binding to intracellular proteins, and apoptosis.4 The most feared complications of CO poisoning survivors are persistent and delayed neuropsychiatric sequelae (PNS and DNS). These can range from mild intellectual impairment to Parkinsonian syndrome to seizure disorders.6,7 DNS have been reported to occur from 3 days to up to several weeks post-exposure.6 Diagnosis The diagnosis of CO poisoning requires the following:4 History of recent CO exposure Presence of symptoms consistent with CO poisoning Elevated COHb level The single most common presenting complaint in patients with mild to moderate CO poisoning is headache,8 occurring in 84% of patients.7  However, symptoms and clinical findings generally are varied and vague. They may also mimic gastroenteritis or viral illness, thus making the diagnosis difficult.6,7,8 Because of the non-specific nature of symptoms, the clinician must maintain a high index of suspicion.4,7 CO poisoning should always be considered when multiple patients present to the ED from a single location with appropriate findings.8 Physical exam is most often non-revealing, but should focus on a detailed neurologic exam, cardiovascular exam, and an assessment for signs of trauma.6,8 A mental status exam may reveal cognitive changes.8 Cherry-red skin is a rare and often post-mortem finding.4,6,7 A blood COHb is very helpful for diagnosis. However, symptoms do not always correspond with the COHb level.1 Also, neither peak nor ED levels correlate well with severity of poisoning or illness8 or with outcome.9 Importantly, a patient may have toxicity even with a normal level depending on the timing of exposure, relative to sampling, degree of exposure, and any oxygen therapy prior to sampling.8  Nevertheless, the following levels, do suggest possible CO exposure:8 >3% in non-smokers >10% in cigarette smokers Pulse CO-oximetry Standard pulse oximeters cannot distinguish the wavelengths of O2 and CO-bound hemoglobin, but more novel devices can measure CO separately.6 Studies are conflicting on the reliability of pulse CO-oximetry. One study found a negative predictive value of 100%, identifying 17 patients with CO poisoning out of 1,578 patients.10 Using the ROC, the optimal cutoff was 6.6% for both smokers and non-smokers. The authors of this study advocate the use of pulse CO-oximetry to screen large numbers of patients. Despite this, most studies suggest that it is useful for more rapid diagnosis but must always be followed by a blood COHb for confirmation, as false negatives occur at an unacceptably high rate.11,12,13,14 One study noted that pulse CO-oximetry was only accurate if the SpO2 is >85%.15 Adjunctive Testing8 -ECG and cardiac monitoring due to potential risk of myocardial ischemia and dysrhythmia -Cardiac biomarkers for ECG changes, symptoms of ischemia, history of CAD, or age >65 -Pregnancy test -For intentional exposure: acetaminophen and salicylate levels -Venous or arterial COHb (no relevant clinical difference between arterial and venous COHb levels, with 95% of samples falling in the range 2.4% to -2.1% of each other)6,16 – Arterial blood gas (ABG) should be done if needed for another reason, but not necessary just for CO toxicity -Severe metabolic acidosis correlates with a short-term mortality rate in CO-poisoned patients. If the source was a fire, consider concomitant cyanide (CN) poisoning. -Lactate levels do not correlate with severity of poisoning but may be useful in possible CN toxicity as well as in sick patients with very high CO levels Management The goal is removal of the CO as soon as possible. The mean half-life of COHb is 320 min on room air, 80 min on 100% O2 at one atmosphere, and 23 min on 100% O2 at three atmospheres in a hyperbaric chamber.5 Treatment thus begins as soon as possible with high flow, 100% oxygen, either by mask or endotracheal tube.4  The O2 should be continued until the COHb is normal (<3%) and the patient’s signs and symptoms have resolved, usually for about 6 hours.6 The use of hyperbaric oxygen (HBO), defined by the Undersea and Hyperbaric Medicine Society as breathing 100% oxygen at 2-3 atmospheres,6 is controversial. The mortality of CO-poisoned patients presenting to a hospital is about 3%, and to date, no study has clearly shown a reduction in mortality with HBO. Therefore, the goal of HBO therapy is the prevention of long-term and permanent neurologic dysfunction.4 A 2011 Cochrane review looked at six randomized controlled trials (RCTs) with a total of 1,361 patients. Of the six trials, two found benefit of HBO for the reduction of the incidence of DNS at one month, while four others did not find this benefit. One trial actually found worse outcomes with two vs one HBO treatments, suggesting that in some circumstances HBO might even worsen neurologic sequelae. These authors concluded that there is insufficient evidence to support the use of HBO for treatment of patients with CO poisoning.  Although they acknowledge that many experts in the hyperbaric medicine community strongly advocate that it has been established as effective, the reviewers maintain that more placebo-controlled clinical trials are warranted. 9 A 2008 American College of Emergency Physicians (ACEP) clinical policy makes similar conclusions:17 HBO is a therapeutic option for CO-poisoned patients; however, its use cannot be mandated. No clinical variables, including COHb levels, identify a subgroup of CO-poisoned patients for whom HBO is most likely to provide benefit or cause harm (controversial; syncope patients likely benefit). Emerging Therapies Treatment of carbon monoxide poisoning with hyperbaric oxygen and therapeutic hypothermia18 A

Originally published at Pediatric EM Morsels on March 6, 2015. Reposted with permission. Follow Dr. Sean M. Fox on twitter @PedEMMorsels Fortunately, the critically ill child is not as common in the Emergency Department as the critically ill adult. Unfortunately, when the critically ill child does arrive, it can be challenging to recognize him/her initially. This can lead to delays in resuscitation care. Even at the extreme point of being pulseless, children can be tricky (SeePalpation of Pulse). Then there is always the challenge that having to account for the effect that age has on normal vital signs (See Blood Pressures).  Often, though, by focusing on the Basics, we can met the challenge of detecting Pediatric Shock and act aggressively to treat it! Pediatric Shock Broadly speaking, shock is the state in which there is a failure to meet the metabolic demands of the body leading to anaerobic metabolism. (Mtaweh, 2013) Often categorized as: Hypovolemic Cardiogenic Distributive Toxin mediated – Septic Hypersensitivity reaction – Anaphylaxis Loss of sympathetic tone – Neurogenic Pediatric Shock: A Challenge The diagnosis is initially suspected based upon clinical exam. There is no lab value or “test” that defines shock. (See Lactate) Clinical Findings: Tachycardia Must account for age-adjusted values! Often children present with elevated heart rates without overt illness. Poor Capillary Refill Normal capillary refill can vary with age and is influenced by the environment. (Schriger, 1988) The initial cap refill in the ED, may artificially affected by the pre-hospital environment. Peripheral Pulse Quality Altered Mental Status Cold/Mottled Extremities Poor Urine Output Not likely useful in the initial assessment in the ED. If the patient is “hanging out” in your ED for some time, monitor this! Of these clinical findings, only Altered Mental Status and Poor Peripheral Pulse Quality was associated with development of Organ Dysfunction. (Scott, 2014) No single finding defines shock, but the absence of all of them is reassuring. Pediatric Shock: The Shock Index The Shock Index (Heart Rate / Systolic BP) has been shown to be useful in detecting adult patients with shock. There is evidence that the Shock Index can be useful in pediatric patients also. (Yasaka, 2013; Rousseaux, 2013) Since, pediatric vital signs alter with age, it would make sense to have a“adjusted” tool. (Acker, 2015) Using standard heart rate and systolic BP values for age ranges, Maximum Normal Shock Index values were calculated. Shock Index, Pediatric Adjusted (SIPA) 4-6 years = 1.2 6-12 years = 1 > 12 years = 0.9 Comparing the patient’s actual HR / Systolic BP to the SIPA was shown to perform better and identify those most severely injured following blunt trauma. (Acker, 2015) Obviously, this may not apply to all pediatric patients presenting with shock, but I do like the concept of utilizing Basic information that is age adjusted. Consider utilizing this tool as another method to help find those subtle presentations of shock.  Remain Vigilant! References Acker SN1, Ross JT2, Partrick DA3, Tong S4, Bensard DD5. Pediatric specific shock index accurately identifies severely injured children. J Pediatr Surg. 2015 Feb;50(2):331-4. PMID: 25638631. [PubMed] [Read by QxMD] Scott HF1, Donoghue AJ, Gaieski DF, Marchese RF, Mistry RD. Effectiveness of physical exam signs for early detection of critical illness in pediatric systemic inflammatory response syndrome. BMC Emerg Med. 2014 Nov 19;14:24. PMID: 25407007. [PubMed][Read by QxMD] Dellinger RP1, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, Sevransky JE, Sprung CL, Douglas IS, Jaeschke R, Osborn TM, Nunnally ME, Townsend SR, Reinhart K, Kleinpell RM, Angus DC, Deutschman CS, Machado FR, Rubenfeld GD, Webb S, Beale RJ, Vincent JL, Moreno R; Surviving Sepsis Campaign Guidelines Committee including The Pediatric Subgroup. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med. 2013 Feb;39(2):165-228. PMID: 23361625. [PubMed] [Read by QxMD] Mtaweh H1, Trakas EV, Su E, Carcillo JA, Aneja RK. Advances in monitoring and management of shock. Pediatr Clin North Am. 2013 Jun;60(3):641-54. PMID:23639660. [PubMed] [Read by QxMD] Yasaka Y1, Khemani RG, Markovitz BP. Is shock index associated with outcome in children with sepsis/septic shock?*. Pediatr Crit Care Med. 2013 Oct;14(8):e372-9. PMID: 23962830. [PubMed] [Read by QxMD] Rousseaux J1, Grandbastien B, Dorkenoo A, Lampin ME, Leteurtre S, Leclerc F.Prognostic value of shock index in children with septic shock. Pediatr Emerg Care. 2013 Oct;29(10):1055-9. PMID: 24076606. [PubMed] [Read by QxMD] Schriger DL1, Baraff L. Defining normal capillary refill: variation with age, sex, and temperature. Ann Emerg Med. 1988 Sep;17(9):932-5. PMID: 3415066. [PubMed] [Read by QxMD]

Check out our latest in our D-List Superbugs series of rare cases caused by rare bugs. EM docs need to have these in their differential as it can cause national morbidity/mortality!

Important background and latest evidence on treatment of TCA overdose