sources from Dr. Marc Kanter’s All NYC EM Conference lecture, enjoy:
sources from Dr. Marc Kanter’s All NYC EM Conference lecture, enjoy:
Pelvic structures are held together by the strong ligamentous connections surrounding it; this is disrupted in pelvic fractures. Keep in mind that the internal iliac vessels and the lumbosacral plexus are intimately associated with posterior pelvic ligaments.
MORTALITY RATE 15-25% for closed fractures, as much as 50% for open fractures… most commonly caused by hemorrhage. The pelvis can hold up to 3-4 liters of blood (nearly HALF your body’s blood volume!)
ASSESSING THE PELVIS
Inspection for ECCHYMOSIS; it can point you towards a bleeding pelvic fracture:
Check for GROSS HEMATURIA – 21% of males and 8% of females.
Check the vagina and rectum to rule out OCCULT OPEN FRACTURES … if so: abx are imperative.
Apply gentle rotational force on each iliac crest
PERFORM THIS ONLY ONCE! DO NOT ‘ROCK’ THE PELVIS!
low sensitivity for detecting instability Get a bedside pelvic x-ray
RESUSCITATION – CABDE (worry about those catastrophic bleeds).
Consider massive transfusion!
PRBC:FFP:Platelets ideally should be transfused 1:1:1
The purpose of a pelvic binder is to CONTROL BLEEDING. It should be centered over the GREATER TROCHANTERS. Do not place over iliac crest/abdomen. Augment with internal rotation of lower extremities and taping at ankles/knees.
The most commonly used system is the young-burgess system that organizes fractures by direction of the impact force:
So when you check your pelvis x-ray, quickly MEASURE to see if there is >2.5cm displacement of the symphysis pubis and >1cm displacement between he sacroiliac joints! This may not only point you towards disposition (surgery vs. conservative management) but also indicates to what degree of bleeding to expect. More displacement = More sheering of vessels.
Keep in mind that 80-90% of pelvic fracture bleeds are venous. Yes, they may be brisk bleeds that present to your trauma room hypotensive, but they can also be slow bleeds. So if your patient stays in your ER longer than intended, make sure you get serial H/H’s.
Total five species (Zaire to have the highest mortality – named after the country in which it was first discovered)
Category A Bioterrorism Agent – Agents with High transmission/dissemination and high mortality – along with Small Pox and the Bubonic Plague.
Discovered in Zaire (or current day Democratic Republic of Congo) in 1976. Named after a tributary that branches off of the Congo River that was near the site of initial outbreak.
Since 1976, there have been 14 outbreaks of Ebola Virus (including current). All have been in either in Zaire/DRC, Gabon, or Sudan.
Unclear however likely secondary to animal vector. Original host thought to be bats as they have frequently been isolated to carry the virus without actually being affected. Likely bat drops a piece of partially eaten fruit, drops it on the ground, which then other animals consume humans hunt for bushmeat…
Body fluid contact with either open skin or contact with any mucosa. Can be carried in serum, tears, urine, saliva, semen, vaginal fluids. Thought to last in sperm even post infection. Infections go up once patients get admitted to hospitals secondary to close contact. Proper personal protective equipment and hygiene is paramount to preventing spread.
Virus can invade any cell in the body however preferentially attacks three:
Keep in mind there is an incubation period ranging from 2-21 days.
High fever >101.5, malaise, asthenia (weakness), myalgias, nausea/vomiting, diarrhea, loss of appetite, joint pains, melena, rectal bleeding, vaginal bleeding, bleeding from gums, conjunctival hemorrhage.
Further down the road Internal/external hemorrhage, rashes including hemorrhagic vesicles/bullae, petechiae, maculopapular rash
Serum/Plasma/ or Whole blood minimum of 4ml shipped refrigerated or frozen on ice pack/dry ice (no glass tubes) as a Category B diagnostic specimen to the CDC.
(1) Percutaneous OR mucous membrane exposure or direct skin contact with body fluids or a person with a confirmed or suspected case of EVD without appropriate personal protective equipment.
(2) Laboratory processing of body fluids of suspected or confirmed EVD cases without appropriate PPE or standard biosafety precautions. Thromobcytopenia can develop over time.
(3) Participation in funeral or other direct exposure to human remains in the geographic area where the outbreak is occurring without appropriate PPE.
(1) Spent time in facility where EVD patients are being treated (people not directly involved in patient care, or if involved in patient care used PPE).
(2) Household members of an EVD patient without high risk exposure.
(3) Persons who had direct unprotected contact with bats or primates from EVD affected countries.
Consultation with local and state health departments is recommended. Stay safe, and have a high index of suspicion.
35 yo F presents to your Resus Room. She’s hypotensive, and not really responding to fluids, and have tried almost all of your pressors. You find out from her accompanying family members that she’s an asthmatic, steroid dependent, and hasn’t been able to make her insurance payments on time as of recent.
What’s going on? (hint: adrenal insufficiency)
A brief reminder of the adrenal gland:
Synthesizes steroid hormones (glucocorticoids – cortisol, mineralocorticoid – aldosterone, gonadocorticoids – testosterone, estrogen) in the cortex and catecholamines (epinephrine, norepinephrine, dopamine) in the cortex.
Primary Adrenal Gland Insufficiency = Addison’s
-destruction of > 90% of adrenal glands
-Results in decreased cortisol and aldosterone production
-causes: autoimmune destruction, hemorrhage (from use of warfarin,sepsis, trauma), tumor (breast and melanoma), infection (HIV, Tb, meningococcemia) or inflammatory process.
-In US 70% of primary AI is due to autoimmune disorders. Can be isolated or associated with polyglanduar autoimmune syndrome (PGA) type I or II.
–About 20% of HIV patients eventually develop adrenal insufficiency, most common infectious cause in US. Worldwide most common infectious cause is TB.
Secondary Adrenal Gland Insufficiency
-insufficient production of ACTH. Occurs following disorders in the hypothalamic–pituitary axis, when CRF and/or ACTH fails to be secreted.
–most common cause is suppression of HPA axis over time due to long term therapy with pharmacologic doses of glucocorticoids.
-other causes: destruction or dysfunction of the pituitary (pituitary disease, head trauma, postpartum pituitary necrosis- Sheehan Syndrome)
-mineralocorticoid (aldosterone) function intact, loss of glucocorticoid (cortisol) activity
Tertiary Adrenal Gland Insufficiency
-hypothalamic disease and suppression of CRH
The life–threatening exacerbation of adrenal insufficiency due to increased physiologic demand (infection) or decreased supply (discontinuation of steroid therapy) of cortisol. Usually occurs in response to major stress: MI, sepsis, surgery, major injury, trauma.
GI: abdominal pain, vomiting and diarrhea
CVS: dehydration, hypotension, refractory shock, poor response to inotropes/pressors
TREATMENT OF ADRENAL CRISIS
–fluid resuscitation (recommendation is D5NS for both hyponatremia and hypoglycemia)
-reversal of electrolyte abnormalities
–high dose hydrocortisone (100mg IV Q6 hrly): provides both glucocorticoid and mineralocorticoid effects
-IV Dexamethasone 4mg may be given if the rapid ACTH stimulation test will be part of diagnostic workup
–vasopressors in patients unresponsive to fluid resuscitation (norepinephrine, dopamine, phenylephrine preferred)
Handoff = Signout = Dangerous
It is well known that patient handoffs are a dangerous time for patients. Information is exchanged and whenever this happens, inevitably something gets lost in the mix.
What can you do to help your patients? Have a system. Any system really, but just having a system in place to signout or handoff patients in a systematic way will reduce medical errors and keep your patients safer. There are numerous systems out there. JCAHO and WHO use SBAR. Our friends and UNM (University New Mexico) use PLAN ED. Here is their policy.
All providers should use the same structured format for handoff presentations in order to facilitate the consistency and completeness of communication among providers and nursing staff.
General Handoff Guidelines:
Proven Techniques for Effective Handoffs
Other General Recommendations
Approximately 0.5% of all patient visits to the Emergency Departent (ED) are acute scrotal pain. The differential is long, and includes epidiymitis, orchitis, testicular torsion, torsion of the testicular appendage, testicular trauma, and herniation of abdominal contents into scrotum. In the ED, we are most concerned with testicular torsion, testicular trauma, and herniation. As they say in CVA, time is brain. In this case, TIME IS TESTICLE. This article focuses on evaluation of acute scrotal pain for torsion, as well as the application of bedside ultrasound to evaluate for testicular torsion.
Torsion occurs when the spermatic cord twists around its axis, cutting off vascular flow to the testicle and surrounding structures in the scrotum. Bedside testicular ultrasound can be a very useful adjunct to the history and physical exam in evaluating a patient for torsion. First, IV access should be obtained for laboratory analysis and most importantly to provide analgesia. A urinalysis should also be obtained if possible. Once analgesia is achieved, the patient should be in the supine position with legs spread apart. Ideally the scrotum should be supported with a sling fashioned from a towel and the penis should be covered with a towel that is taped to the abdominal wall (or the patient can be asked to support his penis in a cephalad position). A high-frequency linear ultrasound probe is then applied perpendicular to the penile shaft to obtain transverse view of the scrotum.
In this “saddle view,” both testicles can be viewed in the same window, as in the following picture:
The definitive treatment for torsion is surgery, so in the ED, we are concerned solely with identifying patients who are immediate candidates to go to the OR. As such, on bedside ultrasound, we want to identify patients with a testicle that has decreased or absent blood flow. Change the settings on your ultrasound machine to “doppler” or “color doppler” and first slide the probe while staying in transverse view to the unaffected testicle. You should see multiple pulsations in both red and blue color throughout the testicle signifying vascular flow. It doesn’t matter whether you have more red or more blue. The key is to have a baseline of “normal” vascular flow in your patient so as to compare to the affected testicle.
Next, gently slide the probe (again while staying in transverse view) to the testicle in question. You are looking for a demonstrable reduction or absence in vascular flow compared to the unaffected testicle. In the following image, there is clearly a reduced flow to the right testicle in this patient compared to the left.
Again, bedside ultrasound for testicular torsion should be used as an adjunct to the physical exam and a good history taking. Absence of cremaster reflex remains the most sensitive sign (90-100%) in diagnosing torsion. Complete ultrasound evaluation of the acute scrotum is obviously much more comprehensive than what I have outlined above, but is beyond the scope of both this article and the purview of the emergency physician. However, visualized absence of vascular flow on bedside ultrasound should prompt immediate urology consult and preparation for the OR.
For more info on scrotal ultrasound: http://www.sonoguide.com/smparts_testicular.html
The patient with undifferentiated dyspnea always presents a unique challenge to the emergency physician (EP). That challenge is compounded when that patient becomes unstable or is crashing and the EP cannot quickly identify the problem using traditional available modalities: EMS report, talking to family, initial physical exam, STAT EKG and portable CXR, and the labs are still in progress.
Call it whatever you want – thoracic/chest/lung ultrasound… it has been around for a while, yet EPs are still unfamiliar or daunted by its readily available application to help them with the undifferentiated dyspnea patient. Its use for identifying PE (right heart strain), pneumonia (hepatization of pulmonary parynchema), and tension pneumothorax (lack of lung sliding/stratosphere sign) have been well-described.
Here, I focused on use of lung ultrasound to quickly identify pulmonary edema/acute CHF as a potential cause of dyspnea, focusing on its advantages over traditional modalities.
An all too-common clinical scenario: 60 YO M with PMHx of DM, HTN, COPD/asthma (not on home O2) and ESRD on HD who presented from home with acute dyspnea. EMS noted a very high BP, 220/100. Initial lung auscultation revealed reduced air movement bilaterally (“tight chest”) with scant expiratory wheezing. O2 saturation was 89%. Portable CXR was interpreted as “unremarkable.” Treatments with albuterol/atrovent and IV methylprednisone were stared for presumed COPD/asthma. Patient noted interval improvement, but on reassessment began to acutely decompensate. The resuscitation team was setting up for rapid sequence intubation; thankfully an ultrasound machine was bedside. Using the phased-array “cardiac” probe, the team leader placed visualized something close to this:
With the probe held in place and slightly rocked from side-to-side multiple shimmering lines such of these were seen extending from the pleural line extending all the way down to the bottom of the screen. Known as “b-lines,” they represent interstitial fluid, or pulmonary edema, and are pathological.
To qualify as a B-line, the following criteria should be met:
The team recognized the aforementioned, applying BiPAP and giving an IV dose of Lasix, with steady improved. By the time the lab tests came back the patient was feeling much better… BNP was >3000 .
This scenario is interesting and common – lung ultrasound was more useful than traditional lung auscultation and CXR, both of which lagged the real-time ultrasound results.
The lesson learned for us was to not wait next time to grab the ultrasound and put the probe on the patient. And secondly, to not use the lung ultrasound as a last resort, but as part of the initial physical exam to quickly differentiate the cause in an acute dyspneic patient.
Sources for images: http://crashingpatient.com/ultrasound/lung-ultrasound.htm/
Beta-Adrenergic antagonists are used to treat hypertension, ischemic heart disease, heart failure, arrhythmias, migraine headache, tremor, portal hypertension, aortic dissection… the list goes on to da break of dawn.
Hypotensive and Bradycardic?
1.) ABCs – no surprise here.
2. IV Glucagon: initial bolus 5mg IVP over 1 min, can be repeated in 10-15 minutes. If changes noted in HR – start drip at 2mg-5mg/hour. Give antiemetics before administration of glucagon.
3. IV Calcium
Ca Chloride – Central line – 1g of 10% — to be repeated up to 3g
Ca Gluconate — Peripheral line – 30mL of 10% to be repeated up to 3g
Monitor Ca levels q 4-6 hours; lethal iatrogenic overdose have been reported.
4. Vasopressor: Epinephrine 1mg/min
5. High dose Insulin/Glucose – remember back to med school – insulin’s physiology involves intracellular calcium utilization; we’ll spare you today though:
1 unit/Kg bolus following by 1 to 10 Unit/kg/hour
A hemodynamic response is delayed for 30 to 60 minutes
Monitor glucose and potassium (we do use insulin in hyperkalemia therapy after all) every 30 to 60 minutes
6. Lipid Emulsion Therapy – check out the physiology mentioned above. BBs love lipids; this therapy tries to coax them out of the body’s tissue and into the emulsion
7. Activated Charcoal: 1g/kg by mouth or NGT one to two hours after ingestion
8. Hemodialyis: effective only with overdose of hydrophilic minimal protein bound beta blockers – we’re looking at you, Atenolol.
– Bradycardia (HR <60) can be caused by SA & AV nodal disease
In patients with symptoms of instability (chest pain, AMS, hypotension)… remember: ABC’s, IV, O2, monitor.
Mobitz type 2 or greater are dispo’ed to CCU (AV blocks may deteriorate into complete block).
Only people to send home are people without comorbidity and received no urgent intervention