Brit Long

An update on the medical clearance of patients presenting to the ED with primary psychiatric complaints. What tests are actually helpful?

An update on the cause, pathophysiology, diagnosis, and management of Lemierre’s syndrome

Author: Brit Long, MD, CAPT (EM Resident Physician at SAUSHEC; USAF, @long_brit) // Editors: Jennifer Robertson, MD and Alex Koyfman, MD (@EMHighAK) Case: A 62 year-old female is brought by paramedics into the emergency department with scald burns to both forearms. The paramedics mention that the patient was cooking with grease when, after briefly turning away from the stove, a fire erupted. As the patient tried to extinguish the fire, she sustained partial thickness burns to the forearms, totaling close to 4% TBSA (total body surface area). The patient quickly doused her arms in cold water and called 911. The primary and secondary exams reveal nothing other than the burns to the forearms. You update her tetanus and provide pain control. However, burn management remains necessary. Following is a brief summary of the classification, pathophysiology and management of burns. In addition, the use of silver sulfadiazine (SSD), previously considered a staple in burn care, will be discussed. Burns are classified by their depth and size and must meet specific criteria to be classified as minor. Minor burns include partial thickness burns < 10% TBSA in patients 10-50 years (yrs) old, partial thickness burns < 5% TBSA in patients < 10 yrs or > 50 yrs old, or full thickness burns < 2% TBSA. Additionally, these burns must be the sole injury and should not include the face, hands, perineum, or feet. They must also not cross major joints or be circumferential. If a burn does not meet the above criteria, then it is classified as a major burn. In the cases of severe burns, patients should be referred to a burn center. The vast majority of burns are minor and can be managed as an outpatient.1,2 Burns involve a dynamic process in the affected tissues. They consist of three areas of injury: zone of coagulation, zone of stasis, and zone of hyperemia. The zone of necrosis is irreversibly damaged, while the zone of stasis can fully recover if adequate care is provided. 3    Local burn treatment includes cooling, cleansing, and debridement of the wounds upfront. However, no consensus on topical treatment currently exists. Usually superficial burns and superficial partial thickness burns (such as sunburns) do not require any topical agent. 4,5 Primary Levels of Burns Care: Cooling of the burn is important in initial wound care as it provides pain relief and decreases injury size.6,7 First, remove any loose clothing, jewelry, or debris. Mildly cool water of about 50 to 60°F should then be used to cool the burn. Sterile saline soaked gauze may also be applied. Do not use ice directly on the wound, as this can actually cause the injury to increase in depth and size. Cleansing and debridement involve removing loose, necrotic tissue. Mild soap and water should be used for cleansing the wounds. Debridement is completed with moist gauze or cotton. This is an important step of burn care, as adequate debridement allows you to view the extent of the injury.3,7,8 If patients undergo any debridement, please be liberal in treating pain. Small blisters are usually left intact, while large open blisters are often debrided. However, debridement of open blisters is controversial and is often institutionally dependent. Large blisters can hinder healing, range of motion, and evaluation of burn depth. Thus, most centers and reviews recommend debridement of sloughed / necrotic skin and ruptured blisters. Topical agents and/or dressings are then typically applied. The surface areas of the burn provide a tremendous medium for bacterial growth and infection. However, selecting the proper agent can be difficult as is usually due to institution culture and cost.3,7,8 One of the most common agents used is silver sulfadiazine (SSD). It is a thick white cream applied one to two times per day. Historically, it was thought to function by decreasing bacterial colonization of the wound. This cream does have antibacterial activity, but there are no well-designed trials that demonstrate improvement in wound healing or reduction of infection. Plus, there are multiple adverse effects, which will be discussed shortly.5 How does SSD actually work? SSD creates a pseudoeschar around the wound, which can actually cause microbial colonization around the outer edges. This pseudoeschar requires removal at the edges to allow wound monitoring and skin growth. Once new skin growth, or re-epithelialization, begins, SSD should be stopped. SSD has also been observed in studies to be ineffective in wounds greater than 50% of total body surface area, especially with Gram negative bacteria.5,9-11 SSD can’t be used in women who are pregnant or breastfeeding. It should also be avoided on the face or around the eyes, as it can cause significant ocular toxicity and scarring. It is also toxic to pediatric patients under the age of two months.5, 9-11 What does the research on SSD actually show? A 2008 Cochrane review demonstrated that SSD delays wound healing time and increases the need for dressing changes and the authors provide evidence for other treatment options. 5 Similarly, a 2006 article by Hussain et al showed that there is no direct evidence of improved healing or reduction in infection by using SSD.9 What can we use instead of SSD for treating superficial burns?  There are multiple options. *Combination antibiotics – Polysporin contains bacitracin and polymyxin B, usually used for superficial burns involving the face and perineum. This is a great option, as polysporin is nontoxic. However, it is not effective for MRSA or deeper wounds.5,12 *Mafenide – This functions as a carbonic anhydrase inhibitor and is applied once to twice per day as a cream. It does have a low risk for rash and pruritus and is effective in treating infections.5,13 However, a common adverse effect is that it can result in metabolic acidosis. Chlorhexidine – This is often used in combination with a gauze dressing, and it does not interfere with wound re-epithelialization. It is also long-acting.5 Povidone-iodine – This combines broad-spectrum antibacterial activity with a moist environment via its liposomal preparation. However, it is cytotoxic and delays wound healing. It

A summary on the etiologies of adrenal insufficiency and crisis, with pearls and pitfalls in diagnosis and management.

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

A focused review of the presentation, diagnosis, and management of renal infarction.

It’s a crazy night in the ED, and you are about four hours into your shift. You have just received a new patient with chief complaint of altered mental status coming in via EMS.

Author: Albert Arslan, MD and Anthony Scoccimarro, MD (Resident Physicians, Lincoln Emergency Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)   Prevent and Identify – the ED’s equivalent of Search & Rescue when managing elevated Intracranial Pressures (ICP). The causes of elevated ICP are typically described in the context of Traumatic Brain Injury (TBI), however many other pathologies can benefit from standardized ICP management. Such problems exist either intracranially (edema, hematoma, seizure, etc) and/or extracranially (coughing, fever, hypoxia, hypercarbia, pain, airway obstruction, etc).(1) Tintinalli describes the primary goals in managing TBI: prevent further secondary brain injury, identify treatable mass lesions, and other life-threatening injuries.(2) An estimated 10 million TBI cases lead to hospitalization and death annually.(1) Mortality in severe injuries, defined as a Glasgow Coma Scale (GCS) score of less than 8, approaches up to 60%.(3) In the information-scarce, time-limited environment emergency physicians work in, having a high index of suspicion for elevated ICP while implementing interventions early goes a long way between patient presentation and definitive management. How can we minimize further elevations? There are several stepwise approaches described in the literature. In May 2014, the New England Journal of Medicine released a TBI review, where within Stochetti et al discuss a traditional “staircase approach to the treatment of increased intracranial pressure.” Dr. Scott Weingart confers his “tiered” management in EMCrit Podcast 78; all of these are either linked or referenced below. Historically, there is a wide scope of traditional management, ranging from head of bed elevation (see picture above) to the potential use of steroids, barbiturates, etc. –  these won’t be discussed in this update. Here we discuss the most current analyses of therapies in the elevated ICP patient, via the trusted ABC’s… and D (and a conceptually interesting E). Airway There are two rapid sequence intubation (RSI) premedications frequently discussed. Lidocaine originally gained favor as an RSI pretreatment after several small trials had demonstrated “less of an increase” in ICP during neurosurgical procedures.(4,5) Despite this initial data, recent meta-analyses have shown that there is no clinically significant reduction in ICP with the administration of lidocaine before direct laryngoscopy.(6)  Some sources argue there is little downside to pretreatment, with a potential/theoretical benefit in ICP reduction in patients at risk for secondary brain injury.(7) Fentanyl has been known to be effective at blunting the sympathetic response during direct laryngoscopy. As per Up To Date, “No data exist regarding the effects of fentanyl on the ICP of patients with acute head injuries undergoing RSI.” They also warn to be weary of tenuous blood pressures; either reduce the dose or avoid altogether.(7) There is some promising recent data, as a study from the Journal of Trauma Acute Care Surgery found that in the treatment of intracranial hypertension,  fentanyl infusions achieved “smaller but significant ICP reductions” when compared to osmotic agents.(8) For a more in depth discussion, be sure to check out this previous emDocs update: http://www.emdocs.net/intubating-critically-ill-patient/ Breathing Traditionally, hyperventilation has been known to decrease ICP by up to 25%.(3) A Cochrane Review states “while hyperventilation therapy can reduce ICP after traumatic brain injury, the review of trials found there is no strong evidence about whether this improves outcomes. More trials are needed.”(9) Circulation Another debated topic is the choice of fluids/osmotic agents, namely mannitol and hypertonic saline (HTS). A Cochrane Review states that “mannitol may have a detrimental effect on mortality when compared to hypertonic saline.”(10)  HTS has been shown to be safe and effective for the reduction of ICP while also improving the patient’s hemodynamic status; however, this has not been shown to significantly affect outcomes.(11) Ultimately, neither agent has been shown to be superior.(1) A search of the Cochrane database shows a study in the protocol stage titled, “Hypertonic saline versus other intracranial pressure-lowering agents for people with acute traumatic brain injury;” so stay tuned.(12,13) emDocs also further discusses BP management in the ICP patient in this prior article: http://www.emdocs.net/aggressive-bp-management-patients-ich/ Diameter A relatively new adjunct to consider in traumatic head injury is the ocular ultrasound (US). It is rapid, minimally invasive, and may have reliable diagnostic capability. It may not obviate the need for further testing, but has the potential for earlier recognition prompting earlier therapeutic action. Several studies have examined optic nerve sheath diameter (ONSD) as measured by US compared to CT scan, as wells as invasive pressure measurements.(14,15) The  pooled sensitivity from these studies was shown to be 90% in a meta-analysis from the journal of Intensive Care Medicine.(16) Another meta-analysis from the Journal of Neurosurgery in 2014 found there may be diagnostic utility with ONSD ultrasound, but due to concerns regarding the heterogeneity of the included studies, is not recommended as a standard of care.(17) Ex-Lap Although completely outside the realm of ED management, Joseph et al expands the conceptualization of trauma management by introducing decompressive laparotomy to treat intractable ICP.(18) The hypothesis in short: the body is a circuit of compartments arranged in series. Each compartment has the capacity to become pathologic in the trauma patient, i.e.: abdominal compartment syndrome thoracic compartment syndrome (pneumothorax, tamponade) intracranial compartment syndrome (discussed above) Decompressing one compartment decompresses another. … ok, so it’s not really Exploratory, as much as it is Therapeutic laparotomy. But let’s be honest, you probably won’t remember the mnemonic “ABCDT” when your brain is under pressure. Bottom Line Have a high index of suspicion; not just in the trauma patient. Airway: Use discretion with fentanyl and lidocaine as RSI pretreatments, time-permitting. Breathing: Hyperventilation – not as useful as previously thought. Circulation: Mannitol vs. HTS – still controversial; HTS favored. Diameter: ONSD ultrasound can’t hurt (unless there’s a globe rupture). Ex-lap: food for thought. Further Reading/Listening Dr. Scott Weingart on ICP/Herniation Management and Neurocritical Care Intubations http://emcrit.org/podcasts/high-icp-herniation/ http://emcrit.org/podcasts/neurocritical-care-intubation/ Ocular Ultrasound: http://www.ultrasoundpodcast.com/2012/04/episode-26-ocular-ultrasound-with-chris-fox/ http://sonoguide.com/smparts_ocular.html http://lifeinthefastlane.com/ophthalmology-befuddler-015/ http://www.ncbi.nlm.nih.gov/pubmed/22327166 Dr. Tom Scalea on Cutting Edge ICP Management http://emcrit.org/podcasts/cutting-edge-icp-management/ http://www.ncbi.nlm.nih.gov/pubmed/20580516 http://www.ncbi.nlm.nih.gov/pubmed/23811861 References Stochetti et. al. Traumatic Intracranial Hypertension. N Engl J Med May 2014 370;22. Ma, O. J., Cline, D., Cydulka, R., & Meckler, G.