Massive Transfusion in Trauma
Sundeep R. Bhat, MD
Stanford/Kaiser Emergency Medicine
Exsanguination is a primary cause of death within the first four hours of trauma and is often due to continued blood loss. However, new evidence suggests it may also relate to ongoing coagulopathy. Recent focus has turned to controlling the so-called "coagulopathy of trauma," an entity thought to relate to clotting cascade disruption in the setting of tissue damage and release of inflammatory mediators. This state is worsened by the lethal triad of resuscitation-induced dilution of clotting factors, acidosis and hypothermia.
Trauma literature shows that coagulopathy increases with increasing injury severity scores and is an independent predictor of mortality among trauma patients. Current standards of resuscitation often suggest replacement of clotting factors only after multiple units of blood. However, several studies now suggest 1:1 replacement of fresh frozen plasma (FFP) to packed red blood cells (pRBC).
This ratio was used in combat support hospitals during recent wartime efforts, where a retrospective study of 246 patients showed those receiving the higher ratio of 1:1 FFP:pRBC had only 19% overall mortality, compared with 65% mortality (1:8 ratio) and 34% mortality (1:2.5 ratio). However, the study was limited in its generalizability. A recent review published in the EM literature examined four studies among civilian trauma patients and did not find conclusive evidence to support a higher FFP:pRBC ratio to improve either hospital discharge or mortality.
It remains to be seen what effect this research will have on massive transfusion protocols. For now, an awareness of the current literature will help guide communication between emergency physicians and surgical trauma teams.
- Brohi K, et. al. "Acute Traumatic Coagulopathy." J Trauma. June 2003, 54(6):1127-30.
- Borgman MA, et al. "The Ratio of Blood Products Transfused Affects Mortality in Patients Receiving Massive Transfusions at a Combat Support Hospital." J Trauma. Oct 2007, 63(4):805-13.
- Zehtabchi S and Nishijima DK. "Impact of Transfusion of Fresh-frozen Plasma and Packed Red Blood Cells in a 1:1 Ratio on Survival of Emergency Department Patients with Severe Trauma." Acad Emerg Med. May 2009, 16(5):371-8.
Teresa M. Ross, MD
Georgetown-Washington Hospital Center Emergency Medicine
When seeing new-onset anisocoria (uneven pupils), consider PCA aneurysm. Aneurysm of the posterior communicating artery (PCA or PComm) is a potentially lethal cause of an incidental CN3 palsy - with or without extraoccular muscle involvement.
- Pathophysiology: PCA aneurysms compress the outer nerve fibers of the ipsilateral CN3 as it exits superior to the pons. Outer nerve fibers are pupillomotor, which explains why the ipsilateral pupil can be dilated, while extraoccular muscles (internal fibers) can remain fully or partially intact.
- H&P: Evaluate for headache (possible), pupil size and reactivity (dilated and unreactive), and EOM involvement ( "down and out" eye).
- Work-up: Emergent CT (rule out space occupying lesion), then CTA or MRA.
- Management: Stat neurosurgery consult, control blood pressure and hold blood thinning agents. Ultimately, the aneurysm will need surgical clipping.
- Epidemiology: 5% of ischemic strokes involve the PCA, with an even distribution of male and female.
We welcome your comments and suggestions. Feel free to get in touch with your elected leaders:
Michael Ybarra, MD
Alicia Pilarski, DO
Megan Boysen, MD
Cyrus Shahpar, MD MPH MBA
At-large Board Members
Heather Jimenez, MD
Jennifer Kanapicki, MD
Jeff Pinnow, MD
Ryan Shanahan, MD
Sandra Thomasian, MD
Medical Student Council President
Jamie "Akiva" Kahn
Copy Editor: Teresa M. Ross, MD
Managing Editor: Jody Bath, AAEM/RSA Staff
Special thanks to this month's contributors: Sundeep R. Bhat, MD; Courtney Smiley, MSIII; Veronica Tucci, MD JD; Teresa M. Ross, MD; Ryan Shanahan, MD; Rikin Shah, MSIII; and Karen Serrano, MD.
To All Emergency Medicine Residency Graduates,
Congratulations on successfully completing your emergency medicine residency!
Before you move on, please help share information about your future cities and jobs with other EM graduates and residents.
Enter your information on the AAEM/RSA Career Network: https://ssl18.pair.com/aaemorg/members/aaemcareernetwork/
Thank you in advance for your participation and good luck at your new job!
Heather Jimenez, MD
AAEM/RSA Advocacy Chair
Image of the Month
Sundeep R. Bhat, MD
Stanford/Kaiser Emergency Medicine
EKG 1. An 82 year old male presented to the ED with one day of diarrhea and increasing weakness.
1. What EKG finding(s) is/are present and what diagnosis can you infer?
- Junctional rhythm with Osborne waves, hypothermia
- Peaked T waves, hyperkalemia
- Sinus bradycardia, beta-blocker overdose
- Physiological long QT
[ Answer ]
EKG 2. A repeat EKG obtained after initial intervention.
2. What was the intervention?
- IV fluids, eventual implantable cardioverter defibrillator
- Active rewarming
- Atropine, glucagon
- Calcium gluconate, bicarbonate, insulin, dextrose, kayexalate
[ Answer ]
Answer to Image of the Month Question
EKG 1 Answer: B
The patient's initial serum potassium was 8.6mEq/dL (normal 3.5-5.3mEq/dL) with a serum creatinine of 2.4mg/dL (normal < 1.3mg/dL). The initial EKG shows a ventricular junctional escape rhythm at a rate of 41 with absence of P waves and tall, peaked T-waves throughout several leads.
Tox Talks: Serotonin Syndrome
Courtney Smiley, MSIII
Veronica Tucci, MD JD
University of South Florida Emergency Medicine
Serotonin syndrome is a toxidrome that is characterized by acute mental status change, autonomic hyper-reactivity and neuromuscular abnormalities.1 Patients may present with tachycardia, tremor, diaphoresis, diarrhea, agitation, restlessness and flushing. Physicians must maintain a high index of suspicion when treating patients with these signs and symptoms who have also recently started one or more new antidepressant medications including SSRIs, SNRIs, MAOIs, St. John's Wart or other serotinergic medications including amphetamines, cocaine, dextrometrophan and meperidine. These drugs can work synergistically on the 5-HT1a receptor leading to overstimulation and the classic signs and symptoms of serotonin syndrome.1
Unfortunately, no one test will rule in or rule out the diagnosis. Blood serotonin levels do not correlate well with symptoms and should not be used to diagnose or treat this condition.
Two algorithms exist to aid clinicians with the diagnosis of serotonin syndrome: Hunter's criteria (sens 84%, spec 97%) and Steinbach's criteria (sens 75%, spec 96 %).4 Accordingly, both are diagnostically helpful when key criteria are met, but their low sensitivities are low, leading to misdiagnosis in about 20% of cases.
Left untreated, serotonin syndrome can be fatal. For this reason, all patients with known or suspected serotonin syndrome should be admitted to the hospital or intensive care unit for observation. Immediate cessation of offending medications may result in resolution of symptoms, but additional supportive therapies including IV fluids, muscle relaxants, benzodiazepines and even resuscitation measures may be required for cardiovascular and neurological complications.
Hunter Serotonin Toxicity Criteria: Decision Rules
In the presence of a serotonergic agent:
- IF (spontaneous clonus=yes) THEN serotonin toxicity= YES
- ELSE IF (inducible clonus=yes) AND [(agitation=yes) OR (diaphoresis=yes)] THEN serotonin toxicity= YES
- ELSE IF (ocular clonus=yes) AND [(agitation=yes) OR (diaphoresis=yes)] THEN serotonin toxicity= YES
- ELSE IF (tremor=yes) AND (hyperreflexia=yes) THEN serotonin toxicity= YES
- ELSE IF (hypertonic=yes) AND (temp.>38C) AND [(ocular clonus=yes) OR (inducible clonus=yes)] then serotonin toxicity= YES
- ELSE serotonin toxicity= NO
Source: references 2 & 3
Steinbach's Criteria for Serotonin Syndrome
- Recent addition or increase in a known serotonergic agent
- Absence of other possible etiologies (infection, substance abuse, etc.)
- No recent addition or increase of a neuroleptic agent
- At least three of the following symptoms
- mental status changes (confusion, hypomania)
Source: references 2 & 3
- Wolfson, Allan B, and Ann Harwood-Nuss. Harwood-Nuss' Clinical Practice of Emergency Medicine. Philadelphia, PA: Lippincott Williams & Wilkins, 2001. 1017-1020.
- Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005;352:1112-1120.
- Bijl D. The serotonin syndrome. Nether J Med. 2004;62:309-313.
- "Chest Pain in ER." AMFS Medical Expert Witness Services. Web. 14 Dec. 2009.
Hot Topics in EM: Ketamine
Ryan Shanahan, MD
Johns Hopkins Hospital Emergency Medicine
For those that missed Dr. Mel Herbert's excellent discussion on the use of ketamine in the ED at the 16th Annual AAEM Scientific Assembly, I thought I would summarize it for you here. The basic message is that ketamine rocks and could be considered for "almost" all instances where you need to do a conscience sedation or intubation as long as you are comfortable using it.
As a basic history, ketamine, a derivative of PCP, was synthesized in 1962 during an explosion of efforts to derive some of the benefits of PCP without the "bad trips." It is a widely used drug outside of the U.S. In this country, it is mainly used in the pediatric population for sedation.
Now, for all the reasons that ketamine is wonderful.
Induction for intubation is typically accomplished with etomidate due to its hemodynamic stability. Recently, there has been concern that etomidate can cause a transient adrenal suppression and is of questionable value in sepsis. While studies have found no effect on mortality with single dose etomidate, they do demonstrate a very real effect on adrenal function. Ketamine has no such effects and has been shown to be equally effective for induction anesthesia in multiple studies.
Additionally, in comparison to many other induction agents, ketamine has the wonderful effect of actually raising blood pressure, making it a much better choice in shock than something like propofol. The fear that ketamine would actually increase intracranial or ocular pressures has been revisited. The original paper supporting this theory out of Japan in the 1980s did report this, but also noted that the entire rise could be explained by the increase in blood pressure. More recent reviews have not substantiated a rise in ICP. In fact, ketamine is being re-investigated as a neuro-protectant in brain injury because of its NDMA receptor antagonist.
Ketamine is an excellent bronchodilator, as well, making it ideal for asthmatics who have failed conventional therapy, both in lower "non-disassociative doses" 0.1-0.2mg/kg or even in full doses 1-2mg/kg. Intubation in asthmatics should always be considered as the last recourse because of the high risk of barotrauma associated with the elevated peak and plateau pressures required. A number of case reports have looked at ketamine as a way to avoid intubation in refractory patients with good result. Dr. Herbert states that he is accumulating the world's body of evidence on ketamine, so maybe there will be more literature other than case reports soon.
Finally, for use in conscience sedation, the main fear seems to be an emergence reaction and awakening agitation. Ketamine certainly has been associated with these effects in 10-20% of adults, but their magnitude can be greatly reduced with a low dose of midazolam to tide the process over. Ketamine may never replace the on/off rapidity of propofol, but its use in combination with propofol - cutely known as "ketafol" - has the synergy of rapid onset with more stable hemodynamic properties.
In summary, Dr. Herbert gave an excellent talk at Scientific Assembly that certainly made me rethink a drug that I had previously relegated to second or third on my list. The most important thing with any drug used in emergency situations is familiarity, both for the physician and the staff. While it may be inappropriate to ask for 140mg of ketamine for your next intubation, it is something to think about and possibly bring up with your attendings, nurses and pharmacists.
Case of the Month: Orbital and Facial Trauma
Rikin Shah, MSIII
University of South Florida
A 49 y/o white female presents after physical assault one hour ago. She was struck multiple times with a lead pipe to the head while sitting in a parking lot and lost consciousness. EMS noted severe facial trauma. The patient complains of right head pain and eye pain but denies neck pain.
On arrival to the ED, the patient is awake, but intoxicated and in severe discomfort. Preliminary vital signs are T 97.0, BP 123/84, HR 95, RR 18, GCS: 14, O2 sat: 95%. Her mouth and throat are suctioned for a large amount of dark red blood.
The right pupil is fixed and dilated with a protruding globe and vitreous extruding from the lateral aspect. The patient states she is unable to see and continues to complain of pain. A non-contrast CT of the head, facial bones and cervical spine revealed facial fractures, a small subdural hematoma, globe rupture and an intraconal hematoma compressing the optic nerve.
Due to the extent of cranial damage, ophthalmology recommended emergent surgical intervention to prevent further loss of vision in her only functional eye.4 On admission, neurosurgery consult was pending for evaluation of the small subdural hematoma, and plastic surgery was consulted for the facial reconstruction.
Considerations in Care: "Maxillofacial Trauma"
Although severe facial injuries can be quite impressive and distracting to physicians, it is important, nonetheless, to address life-threatening conditions via resuscitation and the ABC algorithm, focusing on critical conditions and a limited, pertinent history.
Three questions are essential in facial trauma: (1) "How is your vision?" (2) "Is any part of your face numb?" and (3) "Are your teeth meeting normally?" Pain on eye movement, as in the case of our patient, indicates injury to either the orbit or the globe.2 Women should be asked about domestic violence.
The physical exam, particularly palpation, will reveal the majority of facial fractures. After inspecting for classic signs, such as raccoon eyes and Battle sign, palpation of the entire face should be carefully performed. Findings such as subcutaneous air are pathognomonic for a sinus wall or nasal fracture. The eye exam should be performed early, as progressive swelling of the eye lid can limit the exam.
Females with an orbital fracture have a probability of sexual assault or domestic violence exceeding 30%. Indeed, facial injuries account for most ED visits related to domestic violence.3 Moreover, up to 20-50% of facial trauma victims sustain brain injury simultaneously, especially those with upper and mid-face trauma. Periorbital fractures can be associated with globe rupture or blindness. As such, the sight-threatening triad of limited visual acuity, limited visual fields and limited extraocular movement should be taken seriously and evaluated in all patients with facial trauma.3
CT imaging is invaluable for further evaluation of critical facial trauma. They afford a conclusive diagnosis of complex maxillofacial fractures. CT is also useful in assessing the globe and orbital fissures and for revealing hemorrhage (intracranial/subarachnoid, subdural or epidural) or a midline shift.2,5 Overall, blindness occurs in 0.5 to 3% of patients with facial fractures; it is most frequent in patients with Le Fort III (2.2%), Le Fort II (0.64%) and zygomatic fractures (0.45%). Motor vehicle accidents and gunshot wounds account for the majority of cases of vision loss.1
- Zachariades N, Papavassiliou D, Christopoulos P: Blindness after facial trauma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 81:34, 1996.
- Colby K. Management of open globe injuries. Int Ophthalmol Clin. 1999; 39:59.
- Koo, L, Kapadia, MK, Singh, RP, et al. Gender differences in etiology and outcome of open globe injuries. J Trauma. 2005; 59:175.
- Duch-Samper AM, Chaques-Alepuz V, Menezo JL, Hurtado-Sarrio M. Endophthalmitis following open-globe injuries. Curr Opin Ophthalmol. 1998; 9:59.
- Joseph DP, Pieramici DJ, Beauchamp NJ Jr. Computed tomography in the diagnosis and prognosis of open-globe injuries. Ophthalmology. 2000; 107:1899.
Journal Club: CO2 Monitoring During Procedural Sedation with Propofol
Karen Serrano, MD
University of Wisconsin Emergency Medicine
Providing safe and effective procedural sedation and analgesia is a critical skill of the emergency physician. Current guidelines recommend continuous monitoring of pulse rate and rhythm, respiratory rate, blood pressure and pulse oximetry during moderate and deep sedation.1 End-tidal CO2 monitoring is gaining increasing acceptance as a useful adjunct during emergency department sedation. Real-time capnography, which uses noninvasive techniques to measure carbon dioxide concentration in each exhaled breath, has been shown to identify respiratory depression well before any drop in oxygen saturation. As such, it has been hypothesized that end-tidal CO2 monitoring might improve safety during sedation, particularly with agents that cause respiratory depression, such as propofol.
A study in the March issue of Annals of Emergency Medicine addresses this question by investigating whether capnography reduces hypoxic events during emergency department procedural sedation with propofol.2 The investigators randomly assigned 132 adult patients undergoing procedural sedation to a study group using capnography or a control group with blinded capnography. In addition to standard monitoring, all patients underwent nasal-oral end-tidal CO2 monitoring, but in the control group, the monitor screen was adjusted so only the research associate could see it. Sedation was provided with a propofol bolus of 1mg/kg, followed by subsequent boluses of 0.5mg/kg until the desired level of sedation was reached. Hypoxia was defined as SpO2 < 93% for 15 seconds or greater, and respiratory depression as end-tidal CO2 greater than 50mm Hg, change from baseline of 10% or greater or loss of the waveform for 15 seconds or greater.
Results: Hypoxia was observed in 17 of 68 patients (25%) in the capnography group and 27 of 64 patients (42%) in the control group (p = 0.035, 95%CI: 1.3% to 33%). Regardless of study group assignment, all patients who developed hypoxia first exhibited respiratory depression on capnography (sens 100%, spec 64%). The median time between the onset of respiratory depression and onset of hypoxia was 60 seconds (range 5 to 240 seconds). Physician interventions to improve respiratory status were more likely in the capnography group, 24 of 68 (35%) versus 14 of 64 (22%; difference of 13%; 95% CI: -2% to 27%).
This study convincingly shows that hypoxic events during emergency department sedation can be reduced with use of continuous end-tidal CO2 monitoring. Since all cases of hypoxia in this study were heralded by respiratory depression, capnography provides early warning for potential complications and thus can enhance sedation safety. In an associated editorial, Steven M. Green, MD, argues that as such, end-tidal CO2 should become standard of care for ED sedations.
Voicing an opposing view in the same editorial, Jay Pershad, MD, points out that many episodes of respiratory depression reported in this study were self-limited or resolved with simple interventions such as airway repositioning or supplemental oxygen. In addition, 27% of reported capnographic abnormalities were false positives, not leading to hypoxia. More clinically relevant endpoints to study, he argues, would be more serious respiratory adverse events such as need for assisted ventilation, intubation or hypoxic brain injury.
Procedural sedation and analgesia is an important skill in the repertoire of the emergency physician and this study is the first to provide objective evidence that continuous capnography could improve sedation safety. More data is needed to distill out whether the early warning of potential respiratory compromise provided by capnography translates into clinically meaningful measures of improved safety.
- American College of Emergency Physicians. Clinical policy for procedural sedation and analgesia in the emergency department. Ann Emerg Med. 1998;31:663-667.
- Deitch, K et al. Does end-tidal CO2 monitoring during Emergency Department procedural sedation and analgesia with propofol decrease the incidence of hypoxic events? A randomized, controlled trial. Ann Emerg Med. 2010; 55(3):258-263.
AAEM/RSA's Exclusive - A Must Have!
A Focused Review of the Core Curriculum
22 chapters, 225 board-style questions, 79 images...one way to excel!
Answer to Image of the Month Question
EKG 2 Answer: D
A repeat EKG obtained when his serum potassium was 6.2mEq/dL after treatment with calcium gluconate, IV insulin, 50% dextrose, normal saline and kayexalate shows a normal sinus rhythm with a rate of 76 and resolving peaked T-waves. The patient was admitted to the ICU.