Darrius’ December E-shift

Mysterious Epigastric Pain

Chief Complaint – Acute Onset Epigastric Pain for 2 hours

HPI:  32 year old, previous healthy, AAM, who presents to the ER with 2 hours of acute onset epigastric pain.  Reports some nausea.  Denies fever, chills, vomiting, diarrhea, belching, new foods, melena, and hematochezia.  Denies SOB, chest pain, cough, sick contacts, or rash.

PMH: None

PSH: None

Allergies: NKDA

Medications: None

SH: Occ Alc

FH: Non-significant

Physical Exam

Vitals – BP 120/80, HR 90, RR 18, SaO2 99%, 99.5 F

HEENT – wnl

CV – RRR, no murmur

Respiratory – CTA, equal air entry, no w/r/r/

Abdominal – Moderate epigastric tenderness, positive bowel sounds, soft, no guarding, no murphys sign, no mcburneys point tendernss, no hernia

Extremities – no tenderness, swelling, erythema

Neuro – Gross motor/sensation intact

Skin – No rash

Labs

CBC – wnl

CMP – wnl

Lipase – wnl

Lactic Acid – wnl

UA – wnl

Imaging

AAS – wnl

Discussion 

This patient is a healthy male who presents to the ER with 2 hour acute onset epigastric pain.  The patient has physical exam that supports gastritis, unremarkable vital signs, and unremarkable labortatory values.

This patient’s symptoms were relieved with a intravenous dose of morphine and Pepcid.  The patient’s ER course was unremarkable, and the patient remained stable at all times.  The attending requested a CT ABD/Pelvis w/ IV contrast for further evaluation of the patient’s complaint.

CT Abd/Pelvis Result : Acute appendicitis with perforation.

This patient was referred to the surgical service and taken to the OR later on that afternoon.

Teaching Point

This patient presented with low suspicion based on HPI, and physical exam for appendicitis.  However,  this case taught me to be cautious and be sure to rule out emergencies before considering a patient stable for discharge.  In this patient, without CT Abd/Pelvis, there was not thorough evaluation for appendicitis which represents an acute intra-abdominal emergency.   Missing acute appendicitis is also a common reason for ER malpractice cases.

This case changed my way of practicing.  Potentially, all patients who present with abdominal pain should be evaluated for the known life-threatening emergencies of the abdomen before being considered stable for discharge:

1. Ruptured AAA
2. Acute Appendicitis
3. Acute Cholecystitis
4. Acute Pancreatitis
5. Small Bowel Obstruction
6. Obstructing Urolithiasis
7. Diverticulitis
8. Intestinal Perforation
9. Mesenteric Ischemia
10. Diabetic Ketoacidosis
11. Acute Cholangitis
12. Incarcerated Hernia
13. Pyelonephritis
14. GI Bleed

Fahad’s December E-shift

1. Should all patients who present with chest pain and LBBB (new or presumed new) go to the cath lab?

According to the HERO-2 trial, patients with a LBBB actually had a LOWER incidence of enzymatically confirmed acute myocardial infarction, and 30 day mortality rate, then patients who had a STEMI. So, perhaps we need to be more judicious in our diagnostic approach to LBBB in the setting of chest pain. What appears to be more important, however, is the presence of Sgarbossa criteria for st elevation in patients with LBBB. Patients with LBBB who did not have concordance had a lower mortality rate and troponin elevation. However, patients with LBBB and concordance had troponin elevation and 30 day mortality rates that were similar to patients who presented with a STEMI.

Therefore, it would appear that the presence of new onset LBBB is not as critical as the presence of Sgarbossa’s criteria for acute MI.

References

Neeland, Kontos, Lemos. Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. Journal of the American College of Cardiology. Jul 10, 2012; 60(2): 96–105.

2. What is the risk of intracranial hemorrhage with different anticoagulants?

According to uptodate, anticoagulation with warfarin increases the risk of ICH two to fivefold. Anticoagulation with warfarin and aspirin doubles this risk, when compared with warfarin alone. As for the newer agents, (dabigatran, rivaroxaban, and apixaban), they were found to have a much lower risk of bleeding than Coumadin. However, as with Coumadin, the risk of ICH doubles when these agents are combined with aspirin.

So, while it may certainly be the case that the newer anticoagulants have a lower bleeding risk, we should always ask if the patient is also on aspirin, as the combination appears to increase the risk significantly.

Freeman, Aguilar, Weitz. Risk of intracerebral bleeding in patients treated with anticoagulants. Uptodate.com, Last updated October 29, 2013.

Lindsay’s December E-shift

1. Does CT scan contrast really lead to contrast induced nephropathy?

Based on two recent articles published in the journal Radiology, the answer would be no. The first article “Intravenous Contrast Material-induced Nehropathy: Casual or Coincident Phenomenon?” by McDoland et al was published in April 2013. The study looks at a total of over  150,000 CT scans in over 53,000 different patients and compared 1.5 million creatinine levels from this group. What is different in this study compared to prior studies looking at contrast induced nephropathy (CIN) is that this study looked at the differences in presumed risk of CIN and adjusted for them.  The study looked at each patient and placed them in a low, medium, or high risk group based on prescan creatinine ( <1.5, 1.5-2.0, >2.0 respectively) and then used a propensity score to adjust for the confounding risk factors that were present in each group. These risk factors included patients age, baseline creatinine, history of CHF, gender and race, and Charlson score. The Charlson Score looks at numerous comorbities in patients and assigns them to a risk group based on these. It is used in many studies to help stratify risk. Once this was done, the study found no significant difference in serum creatinine levels after CT scans with contrast.

In the second article, “Intravenous Contrast Material Exposure is Not an Independent Risk Factor for Dialysis or Mortality,” also by McDonald et al, the study group of patients was chosen by matching risk factors in each group in a 1:1 ratio and placing them in low or high risk subgroups based on preexisting cormorbities such as diabetes, CHF, or renal failure.. The study then looked at the incidence of acute kidney injury and dialysis or death in the 30 days following exposure. This study also found that there was no increased risk of AKI or dialysis/death in patients who received contrast.

Both studies were single center and retrospectively completed. The number of patients in each study was much larger than any of the study groups in prior studies on contrast induced nephropathy. And no  prior studies have looked at preexisting comorbities as closely as these did. When this is adjusted for, it was found that patients with more premorbid conditions had poorer outcomes regardless of whether or not they received contrast. Of note, at the hospital where these studies were completed, an iso-osmolar contrast dye was used in high risk patients. In all other patients, the low-osmolar dye Omnipaque was used. The studies did not adjust for this difference or look at a possible benefit from using iso-osmolar dye.

2. How do you treat hypercalcemia?

When looking at elevated calcium levels, it is first important to adjust total serum calcium for albumin levels. This is because calcium is protein bound and in patients with low or high albumin, the free calcium amount will not be accurately reflected.

Calcium Level = 0.8(Normal albumin-patient’s albumin) + Patient’s Calcium level

For patients with an adjusted calcium of less than 12 or for those with levels chronically between 12-14, no treatment is acutely needed. For patients with acute increases in calcium to above 12 more aggressive treatment is needed, and for any patient with a calcium above 14, regardless of chronicity, treatment in required.

The initial treatment of hypercalcemia involves three parts. The first is hydration. IV fluids will help decrease calcium levels that may be due to hypovolemia and since calcium is renally excreted, fluids will help remove calcium from the body. If the patient can tolerate, fluids should be given at a rate of 200-300 cc/hr to maintain urine output of 100-150 cc/hr. Saline alone will rarely correct elevated calcium levels on its own, so drugs that inhibit bone resorption are the next step.

Calcitonin is the favored drug because it is safe and non toxic. It decreases bone resorption and increases renal calcium excretion. Its effects are limited to the first 48 hours of management. The dose is 4 units/kg given subcutaneously or IM every 12 hours.

The third step in treating hypercalcemia is to consider giving a bisphosphonate especially if the cause of the elevated calcium is thought to be secondary to metastatic bone cancer. They prevent bone resorption by interfering with osteoclasts. There are several bisphosphonates available, but due to their associated side effects, they should only be given in consultation with a specialist.

3. What is the best way to treat acute low back pain?

The first line therapy for acute low back pain in NSAIDS. Ibuprofen 400-600mg q6hr or Naprosyn 220-500 mg BID for 2-4 weeks are recommended. With this treatment, about 90 percent of acute low back pain resolves. However, recurrence is common and of those that recover, about 50 percent will experience return of symptoms within 6 months. For acute low back pain in the ED, toradol is also recommended and shown to provide good relief of pain acutely.

Tylenol can also be used to treat low back pain. There have only been a few studies done which show NSAIDS to be superior to Tylenol in pain relief. However, caution is advised with Tylenol use due to its hepatotoxicity and the possible concurrent use with other acetaminophen containing products.

In terms of muscle relaxants, studies have found that the use of centrally acting muscle relaxants in combination with NSAIDs provides the greatest relief of pain. There has been no difference found in the efficacy between the different types of centrally acting muscle relaxants. Options include Flexeril 5-10mg TID (start with 5 mg in elderly), Robaxin 1g PO q6hr, or Soma 250mg qHS for maximum of 2-3 weeks are recommended options. Benzodiazepines are not recommended for use as muscle relaxants because they have been found to be significantly less effective than the centrally acting muscle relaxants.

The use of opioids is not routinely recommended. There have been no conclusive trials to show that their use is more beneficial than that of NSAIDs in combination with muscle relaxants. The risk of abuse and dependence also contributes to their use not being routine. It has been found that nearly 45 percent of patients with chronic low back pain are opioid dependent.

Amrita’s December E-shift

1. What is the evidence behind anticoagulation in ischemic stroke in patients with atrial fibrillation?

We see ishemic stroke in patients with new onset atrial fibrillation or in patients who are noncompliant with anticoagulation quite commonly. We get stuck in this dilemma of whether to start anticoagulation in these patients or not. I had a case of this last year and, when I spoke with the neurologist on call, he did not recommend a heparin drip. So, what do the studies say? There have been many studies trying to answer this question dating back to 1983. There was a meta-analysis published in Stroke in 2007 that took a look at 7 trials involving a total of >4000 patients. Mainly UFH or LMWH were used in these trials. Interval time to treatment included less than 3 hrs to within 24 hrs of onset of ischemic stroke. The results included the a significant increase in intracranial bleeding (2.5% vs 0.7%), no significant reduction in recurrence of ischemic stroke (3% vs 4.9%) and a similar rate of disability. Now, not all the trials had the same outcomes. In trials which gave treatment within 3hrs of onset of ischemic stroke, they saw some benefit to treating with thrombolytics. However, there was only 1 study that had this time interval and these results. Definitely, more studies need to be done before we can comfortably start heparin in the ED. Aspirin is still highly recommended in these patients and must be given in the ED. When are anticoagulants started in these patients? The studies say 2-3 days after the stroke is a good time to start oral anticoagulants (warfarin) and ASA.

2. New onset Atrial Fibrillation and anti-coagulation

With emergence of newer LMWH that are a lot of safer with fewer side effects, we are seeing more usage of them for everything including for anti-coagulation in new-onset atrial fibrillation. In a prospective randomized controlled trial published in Annals of EM in 2002, they used Dalteparin to bridge with coumadin and stratified patients based on the onset of A. fib. Below is the strategy they used:

In new onset A fib, they achieved rate control and then stratified patients. If the patients had no other EKG changes after the rate control, they were considered for possible out patient treatment. They found reduced length of stays in the hospital and reduced costs. They concluded the study by saying that more studies ne
ed to be conducted before this approach is used comfortably in the ED. In 2011, a randomized control trial with LMWH (tinzaparin) vs UFH was used. LMWH was found to be just as effective as UFH in reducing ischemic stroke. So, LMWH could be a good alternative to UFH. Something keep in the back of our minds for the future.

Click here for the journal article pertaining to this topic:

Anti-coagulation in ischemic stroke[1]

Ari’s October E-shift

Decompensated Heart Failure from hypertensive emergencies. Is there room for improvement?

We’ve all been working at one point or another and had to take care of someone, usually in resus, that presents with some combination of several of the following: SOB, dyspnea, edema, rales/crackles, blood pressure through the roof, history of CHF, pulmonary edema on chest XR etc. I’m painting an overall picture of decompensated heart failure secondary to hypertensive emergency.

We have a pretty standard management plan depending on how severe they look. Get their pressure down, give some lasix, oxygen, +/- BIPAP, and sometimes (usually) nitro and a nitro drip. For the initial nitro we give a SL which is 0.4 mg (400 micrograms) and a drip started small and titrate it up while carefully monitoring BP for hypotension to the end game of symptom resolution or failure and intubation.  

Lets go over some pathophysiology really quick. Why does any of that work?

Decompensated heart failure can come in two main forms, left and right, systolic or diastolic dysfunction. In markedly hypertensive pts we usually think of systolic dysfunction. There’s a really high afterload, the heart has a hard time pumping against that, and then that all backflows into the lungs, causing pulmonary edema. Keep in mind though, that diastolic dysfunction can also be part of the cause of decompensation. Because of the decreased EF and contractility you can have high end diastolic volumes, high diastolic pressures, and resulting in cardiogenic pulmonary edema. So how does nitro help?

The vascular response to nitroglycerin is dose dependent in nature. At less that 250 mics per minute the main effect is predominantly venodilatory in nature, which helps reduce preload, which can help alleviate some of the systolic dysfunction by helping with contractility. But, more importantly in our scenario, afterload reduction would be more helpful, and that occurs at high doses of more than 250 mics per minute for aterial and venous dilation.

The reason this discussion came about is because I really didn’t sit and think about the doses of meds I was giving and why I was giving them, until a case I had with George, our pharmacist. Usually I’ll give a sublingual, start a drip and the nurses dose it. The dose should be 0.3 to 0.5 micrograms/kg/minute and increases in units of 20 at physician (nursing really) discretion, for a max of 400 mics per minute. Then george asked me why stop there? We know it’s a dose dependent medication, is there room for improvement with even higher doses?

So we sat and talked about a study he was actually part of with using much much higher doses of nitro for this scenario, with better end point outcomes and a very small percent of complications .

Their protocol was to use a 2000 microgram (2 mg) bolus IV while starting the drip for people that failed in initial conservative measures, and then repeat every 3 to 5 minutes at physician discretion, up to 30 minutes and a max dose of 20 mg. That’s a huge amount. Its the equivalent of 50 sublinguals. They would stop with hypotension, chest pain, neuro deficits, intubation etc.

They found that the majority of people got an average 6.5 mg of nitro at three boluses, they were able to cut those drips from 31.7 mics per hour to 23.6, lasix dosing needed was the same. But what they found that was most impressive was that only 13.8 percent needed the endpoint of intubation in their treatment group comparets to 26.7 percent with the standard dosing. Bipap went from 20 percent to 6.9 percent. ICU admission rate went from 80 percent to 37 percent. There was only one patient out of their study with profound hypotension that got every thing shut off and fluids. It was actually a really cool designed study, with good data and physiology and endpoints that made sense to me. George is our in house pharmacist, we can all ask him about it. I think it’s a good study that makes a lot of sense, and if we can avoid a large amount of BIPAP, ICU stays, intubations etc with a small amout of reversible adverse events we should really be thinking about doing this more.

Chris Arnold’s November E-shift

1. Treatment of Acute Gout

Gout is a simple but fairly common cause of pain seen in emergency medicine. It can pose some issues with diagnosis, and treatment especially if the patient has renal disease.

Initial treatment of gout

1. Pain Control! This is a painful condition and NSAIDS, or Colchicine is not sufficient.
2. No benefit in urate lowering therapies (Allopurinol), but do not stop them if patient is already taking.
3. Aspirin is not used to treat acute gout because of the paradoxical effects of salicylates on serum urate, resulting from renal uric acid retention at low doses (<2 to 3 g/day) and from uricosuria at higher doses
4. NSAIDS are primary therapy. No difference between classes. Treatment duration is until symptoms resolve.
5. NSAIDS should not be used in patients with CAD, Chronic Renal Disease, Gastric Ulcers, NSAID intolerance, or patients with ongoing anticoagulation therapy.

Patients with contraindications to treatment with NSAIDs.

1. Colchicine is best therapy if symptoms have started within last 12 hours. The initial dose of 1.2 mg followed by 0.6 mg in one hour. Colchicine should then be continued 0.6 mg BID until resolution of symptoms.
2. Traditionally Colchicine was given as above but 0.6 mg tab was taken every hour until pain resolved or patient developed diarrhea and abdominal cramping (The patient only did this once). Furthermore, AGREE trial showed no benefit with this treatment regimen.
3. Finally Colchicine is contraindicated in patients with advanced renal or hepatic impairment because of risk of toxicity 2/2 decreased clearance.

Patients with Chronic Kidney Disease

1. Glucocorticoids are mainstay of treatment.   Intraarticular injections are acceptable if 2 or less joints are affected and if infections has been ruled out. In most patients with CKD oral glucocorticoids are treatment of choice in the Emergency Department. Prednisone 30-50mg q/day 7-10 days if initial flare, or 10-14 days if a recurrent attack.
2. Caution should be used with glucocorticoids in patients with diabetes as it can cause elevated blood sugar and if necessary patient should be educated of effects and need to monitor blood glucose and increase insulin requirements as needed.

 

2. Treatment and Prophylaxis for Spontaneous Bacterial Peritonitis

I recently had a patient with a GI bleed and a history of ascites. I had believed that I needed to treat them prophylactically for SBP, but could not remember the indications. When speaking to some of the other residents I realized it was a common gap in our knowledge.

Treatment for SBP is indicted if any of the following exist in a patient with ascites after fluid has been obtained and sent for culture.

1. Temperature > 37.8 C/100 F
2. Abdominal pain/tenderness
3. Change in Mental Status
4. Ascitic fluid PMN > 250

If SBP is highly suspected then treatment should begin immediately after fluid has been collected for culture, otherwise it can be postponed until PMN count is available. Treatment should be aimed at common G- bacteria such as E. Coli and Klebsiella. The recommend regimen is cefotaxime 2 grams IV q8 hours. Any third generation cephalosporin is a reasonable choice (since we done have cefotaxime), and if ceftriaxone is chosen the dose is 2 grams/day.

Prophylaxis is indicated in the following settings.

1. Cirrhosis and GI bleeding -> prophylaxis decreased mortality
2. History of SBP. 70% reoccurrence rate within one year.  
3. Cirrhosis and ascites fluid with low protein <1.5 g/dl and CKD defined as Creatinine >1.2, or BUN > 25, Sodium < 130, or advanced liver failure.

Treatment regimens for SBP prophylaxis vary by indication and I have simplified it here.

1. Ceftriaxone 1 gram/day for patients with GI bleeding
2. Patients with a history of SBP should have long term PPx with Bactrim DS.
3. The third group can be treated with daily Bactrim DS or Norfloxacin

Darrius’ November E-shift

Question: Does mild traumatic brain injury (mTBI) associated with loss of consciousness necessitate neuroimaging?

Background: New Orleans and Canadian CT Head Rule are the two most commonly sensitive and specific cited guidelines at identifying patients with mTBI who have clinically important lesions.

Canadian CT Head Rule

• GCS < 15 at 2 hours after the injury

• Suspected open or depressed skull fracture

• Vomiting > 2 episodes

• Physical evidence of basal skull fracture

• Age > 65

New Orleans CT Head Rule

• Headache

• Vomiting

• Age > 60

• Drug or alcohol intoxication

• Amnesia

• Seizure

• Evidence of injury above the clavicles

Other possible indications for head CT in mTBI include anticoagulation, very young age (infants), shunt for hydrocephalus, focal neurologic findings, dangerous mechanism, and penetrating skull injury.

Loss of consciousness for > 5 minutes is an accepted high‐risk indication for head CT on patients with mTBI. There have been cases of patients that did not lose consciousness, could remember everything, and present awake and alert, and yet required ICU care and neurosurgical intervention after head CT demonstrated traumatic injury.

History of fall when compared to MVC produced higher positive head CT findings in patients with mTBI. A fall from any height is suggested as a minor criteria for obtaining head CT in mTBI.

Although most CT scans are negative, missed injuries can contribute to significant morbidity and mortality. Missed injuries are estimated to be 5‐9%.

Cost effectiveness of performing head CT on mTBI patients has been reviewed. Fewer than 10% of patients with mTBI will have positive findings on head CT. More than $20 million could be saved in the healthcare system with an even 10% reduction in the number of head CT’s performed on mTBI patients. However, the cost of resources to observe such patients without imaging may actually exceed the cost of performing head CT on initial evaluation (cost of hospital admission, man power resources needed to re‐evaluate, prolonged observation).

Conclusion: Which patients need CT after mTBI is controversial. Loss of consciousness > 5 minutes is suggested as criteria for obtaining head CT in patients who present with mTBI. CT serves as a poor test for determining the longterm clinical course of patients that present with mTBI – there is significant need for objective measures that can help predict clinical course of patients with mTBI.

References:

Glauser, J. “Head Injury: Which Patients Need Imaging? Which Test Is Best?” Cleveland Clinic Journal of Medicine 71.4 (2004): 353-57.

Lee, B., et al. “Neuroimaging in Traumatic Brain Imaging.” NeuroRX 2.2 (2005): 372-83.

Parma, C., et al. “Unnecessary Head Computed Tomography Scans: A Level 1 Trauma Teaching Experience.” The American Surgeon 80.7 (2014).

Tim’s November E-shift

1. Proparacaine 1:10 dilution for eye pain?

Traditionally discharging patients with proparacaine for eye pain has been verboten, potentially causing complication from abuse including “punctate keratitis, persistent epithelial defects, stromal/ring infiltrates, corneal edema, endothelial damage and ocular inflammation” all of which sound kinda scary, messes with actic fibers and cell membrane stability. Yet recently a number of academic institutions have been sending home patients with a 1:10 dilution of proparacaine from the ED. Should we be adopting this practice, is it the future of eye pain?

Studies I found included a British one of 18 patients, double blinded, sent home with the dilution showing that yes, the dilution is still effective in pain relief compared to placebo with no cornea injuries resulting during the study. While I found several equally small studies, no good consensus article or metanalysis was found during a google scholar search.

Somewhat concerning was an animal trial which showed that although no cell death occurred or change in functionality of the cell, rabbit cornea’s treated with low dose proparacaine for a duration of 24 hours showed change in the morphology of the cells, could not find any animal trials that showed what would happen beyond the 24 hour mark.

Also, even more concerning for me was although I found multiple international case reports of toxic kerotitis from prolonged dilute proparacaine use after dilutional topical proparacaine use. Enough so that even with a number of academic institutions in the US are using such a practice and a few small scale studies show no harm, me myself will not be proscribing dilute proparacaine

Dilute proparacaine for the management of acute corneal injuries in the emergency department. Ian Michael Ball, MD;^* Jamie Seabrook, MA;^† Nimesh Desai, BSc(Pharm), MD;^‡ Larry Allen, MD;^‡  Scott Anderson, MD^*

Comparative Toxicity of Tetracaine, Proparacaine and Cocaine Evaluated with Primary Cultures of Rabbit Corneal Epithelial Cells.   Roberta L Grant, Daniel Acosta

Toxicity of topical ophthalmic anesthetics. August 2013, Vol. 9, No. 8 , Pages 983-988 Michelle Patel and Frederick Fraunfelder. Oregon Health & Science University, Casey Eye Institute, Department of Ophthalmology

Ring Keratitis Associated With Topical Abuse of a Dilute Anesthetic After Refractive Surgery. Yu-Chih Hou, I-Jong Wang Fun-Rong Hu Department of Ophthalmology, National Taiwan University Hospital, Taipei, Taiwan 27 November 2007

Overview of ocular anesthesia: past and present Bryant, Juanita S^a; Busbee, Brandon G^b; Reichel, Elias^c

 

2. Prophylactic antibiotics for bird bites? Which should we use?

I found a number of good case studies with birds causing significant infection. Mycobacterium after a parrot being one, owl attack causing bacteroides and a fatal abscess from a rooster pecking, another weird one with a swan but no specific to bird guidelines or recommendations found. It’s been noted that staph and strep are still the predominant bacteria, multicocida also having been cultured. Recommendations from the best article I found just recommended augmentin with additional culture guided therapy if wounds were nonhealing despite full course antibiotic therapy.

Mycobacterium chelonae/abscessus Infection Caused by a Bird Bite Larson, Jan M. MD*; Gerlach, Sharon Y. MD†; Blair, Janis E. MD‡; Brumble, Lisa M. MD§; Jorn, H. Keels S. MD†; Thompson, Kristine M. MD∥ Infectious Diseases in Clinical Practice: January 2008 Volume 16 Issue 1 pp 60-61

Striges scalp: Bacteroides infection after an owl attack. Davis B, Wenzel RP: J Infect Dis 1992, 165:975–976.

Striges scalp: Bacteroides infection after an owl attack. Davis B, Wenzel RP: J Infect Dis 1992, 165:975–976.

Management of human and animal bite wound infection: An overview Itzhak Brook Current Infectious Disease Reports September 2009, Volume 11, Issue 5, pp 389-395

 

3. What are the recovery expectations for a patient with non penetrating isolated nerve damage?

While it’s never a good idea to give a patient a hard and fast prognosis, many of our patients do ask for guidelines and expectations. The answer of course is ‘it depends’. It depends on age and comorbidities, degree of damage, etc, yet there do exist some basic guidelines based on type of initial injury.

Neuropraxic injuries are the more mild type, due to compression or ischemia. The actual damage to the nerve is focal demylination, no damage to the axon itself. Saturday night palsy is a classic example of this. Recovery is typically excellent with full resolution within hours, day or weeks up to three months at the max.

Axonotemesis injuries actual damage to the axon from trauma typically, a crush injury from blunt trauma or a stretch injury in a fall in which demylination occurs AND axonal damage but with intact endoneurium and perineurium. Nerve undergoes wallerian degeneration but may recover because the existing schwann cells act as a tract and blue print for nerve regrowth.  Recovery pattern is a little weird kinda bimodal. Initial rapid partial recovery is dependant on distal axonal sprouting, with a slower possibly fuller recover over next 4 months although complete recovery is unlikely. Strongly encourage physical therapy on discharge as initial muscle hypertrophy has a surprisingly large beneficial effect on recovery.

Sources, Uptodate and Rosen

Kuper’s November E-shift

Question 1 What is the utility of Echo for a pt with established submassive PE?

Although, the pt with submassive PE (ie hemodynamically stable) is going to be receiving heparin regardless, an echo is a very good thing to get after the diagnosis has been made as it helps to risk stratify your pt. Mortality after submassive PE is linked to several things that could be elucidated on echo. RV strain leads to a two-fold increase in mortality¹ while RV thrombus increases 3 month mortality to 29 vs 14%². Following that logic that you should risk stratify PE pts they also should have a LE duplex scan since the presence of DVT has a hazard ratio of 2.01 for mortality at 3 months. That being said, I’m not sure if they need to stay in the department for either one of these scans.  

¹ ten Wolde M, Söhne M, Quak E, et al. Prognostic value of echocardiographically assessed right     ventricular dysfunction in patients with pulmonary embolism. Arch Intern Med 2004; 164:1685.

²Torbicki A, Galié N, Covezzoli A, et al. Right heart thrombi in pulmonary embolism: results from the International Cooperative Pulmonary Embolism Registry. J Am Coll Cardiol 2003; 41:2245.

 

Question 2 What is the role of thrombolytics in a submassive PE?

This question is complicated, I’m going to break it up into two discrete pt populations to make it manageable.

2a. A pt with submassive PE and RV dysfunction

The PEITHO trial tackled this question and showed that thrombolytics did improve pt outcome initially. Compared with heparin alone, thrombolysis resulted in a reduction in the primary endpoint of death or hemodynamic decompensation at seven days (6 versus 3 percent; OR 0.44, 95% CI: 0.23-0.87). However this improvement came at a cost with 2% vs 0.2% of pts had an ICH. Major bleeding was also reported 11% of pts older than 75 vs 0.6% in the heparin group. Importantly at 30 days there was no difference in mortality a total of 12 patients (2.4%) in the tenecteplase group and 16 patients (3.2%) in the placebo group had died (P=0.42). I take away from this that we need to further risk stratify tenectaplase recipients before we start giving thrombolytics for RV dysfunction.

Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med 2014; 370:1402.

            2b. A pt with a large clot burden

The MOPETT trial addressed this, the randomized pts with a large clot burden defined as computed tomographic pulmonary angiography demonstrating >70 percent involvement with embolism in ≥2 lobar arteries or main pulmonary arteries or by a high probability ventilation/perfusion scan showing ventilation/perfusion mismatch in ≥2 lobes. The study used smaller doses of thrombolytics than previous using 100mg for pt >50kg or 0.5mg/kg for pt <50 kg. They found that:

• Lower rates of pulmonary hypertension (57 versus 16 percent)
• Lower pulmonary artery systolic pressures at 28 months (43 ± 6 versus 28 ± 7 mmHg)
• Faster resolution of pulmonary hypertension (50 ± 6 mmHg versus 51 ± 7 mmHg on admission; 43 ± 6 mmHg versus 28 ± 7 mmHg at 28 months)
• Similar rates of bleeding (0 percent in each group), recurrent PE (5 versus 0 percent), and mortality (5 versus 1.6 percent)

Criticism of this trial centers around the fact that <25% of the participants had any signs of RV strain (so possible a less severe cohort than the PEITHO trial). Also, only 121 pts were enrolled in the study so it needs to be done on a larger scale.

Sharifi M, Bay C, Skrocki L, et al. Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT” Trial). Am J Cardiol 2013; 111:273.

Rosie’s November E-shift

1. What is the significance of scalp hematomas in relation to TBI in pediatrics?

Most children with isolated scalp hematomas and no other significant findings will not have a clinically important traumatic brain injury.  There are certain features that increase the risk, and clinical decision rules have been made to determine who is at risk.  Scalp hematomas can be an indicator of TBI when they appear in younger infants.  In a multicenter observational study of 2998 children < 24 months old with a scalp hematoma, TBI occurred in only 12 patients.  None of whom required neurosurgery or died.  Of 111 patients < 3 months old who underwent CT, 21% had findings of TBI (subdural/epidural, hemorrhage or contusion).  A previously validated clinical score incorporates age, hematoma size, and hematoma location to help stratify the risk of TBI in young infants.

• 3 points indicates increased risk of TBI in infants with scalp hematomas

Risk pts	Patient age (mo)	Hematoma Size	Hematoma location
0	Greater than 12	None	Frontal
1	6-11	Small (barely palpable)	Occipital
2	3 to 5	Medium (easily palpable)	Temporal/parietal
3	0 to 2	Large (very easily palpable)

2. What is the significance of an isolated loss of consciousness in children with minor head trauma?

New data suggest that risk of clinically important TBI that requires neurosurgical intervention, intubation, or hospitalization of at least 2 days is low in the setting of brief, isolated LOC without any other clinical predictors.  In a prospective cohort study of more than 5000 children with LOC after mild head trauma, 0.5 percent of children with isolated LOC plus having no other worrisome features of TBI* had confirmed TBI.  This is in comparison to 4 percent of children with LOC who had met some criteria for being non-low risk for TBI.

*PECARN Head Injury Prediction Rule

Age (years)	Clinical Criteria
< 2	Normal mental status
	Normal behavior per routine caregiver
	No LOC (defined as > 5 seconds)
	No severe mechanism of injury**
	No occipital/parietal scalp hematoma
	No evidence of skull fracture
2 to 18	Normal mental status
	No LOC
	No several mechanism of injury ***
	No vomiting
	No severe headache
	No signs of basilar skull fracture

** Severe mechanism: fall > 3 feet, head struck by high impact object, MVC with patient ejected, death of another passenger, rollover, pedestrian/bicyclist without helmet struck by motorized vehicle.

*** Severe mechanism: same as for children < 2 but fall greater than 5 ft to be considered severe.

                So if a patient met all the criteria for PECARN but still had a brief LOC – they are considered low risk for TBI and do not routinely require neuroimaging. 

 

1. Now that I’ve mentioned PECARN, what are some other clinical decision rules for pediatric and neuroimaging?  And what’s the best?

In Annals of EM (2013), there was a prospective study to evaluate 3 major clinical decision rules in addition to 2 measures of physician judgment for children with minor head injury.  The three rules are PECARN, CATCH, and CHALICE and the 2 measures of physician judgment were (1) estimated of < 1% risk of TBI and (2) actual CT ordering practice.  For all the clinical decision rules, the absence of any features of the rule obviates the need for CT by placing the pt in a low risk category for having clinically significant TBI. See above for PECARN, but here are the other rules:

CATCH – Canadian Assessment of CT for Childhood Head Injury CT of the head is required for children with minor head injury* and any one of the following: High risk (need for neurologic intervention)

1. GCS < 15 at 2 hours after injury
2. Suspected open or depressed skull fracture
3. Hx of worsening headache
4. Irritability on exam

Medium Risk (brain injury on CT)

1. Signs of basal skull fracture
2. Large, boggy hematoma of scalp
3. Dangerous mechanism of injury

*Minor head injury = witnessed LOC, amnesia, disorientation, vomiting, irritability in pt with GCS of 13-15.

CHALICE CT scan is required if any of the following criteria are present: HISTORY – Witness LOC > 5 min – Amnesia > 5 min – Abnormal drowsiness – > 3 vomits post injury – Suspicion of NAI – Seizure after injury in patient with no history of epilepsy

EXAM – GCS < 14 or GCS < 15 if under 1 yo – Suspicion of penetrating/depressed skull injury or tense fontanelle – Signs of BOS # – Focal neurology – Presence of a bruise, swelling or laceration > 5 cm if under 1 yo

MECHANISM – High speed MVA – Fall > 9 ft – High-speed head injury from a projectile.

This was a prospective, single center, cohort study of children younger than 18 years.  Patients included had (1) history of signs of blunt injury to head (2) GCS scores greater than 13 (3) injury within 24 hours of presentation (4) physician concern for potential TBI.  A total of 1009 children were enrolled.  The physician recorded presence of predictor variable associated with each decision rule.  Physicians also recorded their estimate of the likelihood of their patient having a clinical important TBI (percentage between 0-100%) and their actual CT order practice.  In totally, 5 modalities were studied (3 clinical decision rules + 2 measures of physician judgment.

Primary outcome was clinically important TBI, defined as death, need for neurosurgery, intubation, hospital admission greater than 2 nights.  Outcomes were verified through chart review, patients who didn’t undergo CT were followed up to determine if they met any of the outcomes.

In conclusion of the 5 modalities studies, only physician practice and PECARN identified all clinically important with TBI, with PECARN being more specific.  CATCH and CHALICE misclassified a small proportion of patient with clinically important TBI as low risk.  Physician estimation of low risk patients had a sensitivity of 95% and specificity of 68% compared to the PECARN which had a sensitivity of 100% and a specificity of 62%.  CATCH was incompletely sensitive and had the poorest specificity of all modalities.  So in conclusion, if you are going to use one – use PECARN for determining if your patient can be considered low risk for TBI.