49 yo F

The pt is a 49 yo F with a hx of uncontrolled hypertension and heavy smoking, presnting for a week of nausea, vomiting, diarrhea, and now abdominal pain. Pt BIB EMS, found by the to be hypotensive, on arrival to ED, pt is ashen, exrtremely pale, in distress, saying "I cant breath", hyptensive to 80s systolic, tachycardic to 130s. Her abdomen seems distended and is pulsatile on palpation. Ultrasound machine is brough into the room, shows a 9cm structure at and below the umbilicus (AAA? but too low?). Pts vitals improve enough after 2L IVF on pressure bags for her to be taken to CT, she is in the scanner 30min after arrival in ED, vascular surgery contacted before she goes to CT and actually meets her there. Findings are below.

Pt had a ruptured ILIAC artery aneurysm. Her initial pH was 7.07 and lactate 19.5. Hgb 6.2. Upon return from CT, blood was waiting for her, her vitals improved to SBP in 120s and HR  around 100. She was less pale. She was taken to the OR just over an hour after arrival in the ED. Currently in SVTU, doing well as far as I can tell.

68 yo F with left lower face pain and swelling x 5 days

HPI: The pain/edema was initially noted in the left lower lateral face and progressed to include anterior tongue. The patient was tolerating her secretions though it was painful for her to open her mouth. There was no history of oral trauma. No fevers, chills, headache, dizziness, vision changes, skin changes, and shortness of breath.

PMH: Rheumatoid arthritis on Methotexate, Adalimumab, and Leflunomide

PE:

-VS: T 37.1.C; BP: 156/98 mm Hg; HR: 115 beats/min; RR: 18 breaths/min, pulse ox: 96% on RA

-Gen: Well appearing

-HEENT/Neck: left submandibular edema with TTP. No overlying erythema. Tongue with mild distal edema, but no fluctuance; there was no tongue protrusion, trismus or drooling. Full ROM of the neck, with mild pain on neck rotation. No other oropharyngeal edema. Normal dentation without evidence of oral trauma

CT Max/Face W/Contrast (click on image to make bigger): 

Diagnosis????

Answer:

Tongue Abscess. Likley secondary to immunosuppression. Radiologist called to say he had never seen this before and according to the limited literature, it is rare. Less than 30 cases reported in the US.

Backround info: Spontaneous lingual (tongue) abscess is a rare life-threatening medical condition that may result in acute airway obstruction. The rich vascular supply, thick mucosa, and the anti-infectious characteristics of saliva make lingual abscess uncommon. Symptoms of a lingual abscess include tongue pain and swelling, odynophagia, dysphagia, difficulty speaking, changes in voice, tongue protrusion, and fever. 

The responsible organisms are usually normal flora from the oral cavity. The most common cause of a lingual abscess is direct trauma, whether this be from the teeth or a foreign body, and can also occur in association with dental infections. Immunocompromised state is considered a predisposing risk factor.

The differential diagnosis for lingual abscess includes aneurysm of the lingual artery, neoplasm, hemorrhage, infarction, cyst and angioedema. CT scan with IV contrast is generally recommended for improved characterization of the lesion, though it may be difficult to determine the etiology without surgical exploration and biopsy.

The treatment of a TA begins with airway assessment. Once airway stability is confirmed, further management includes broad-spectrum antibiotics to cover oral flora and consultation with either oral surgery or ENT to discuss drainage of the infection. 

Evaluation of Low Risk Chest Pain

Background for the residents: You will be seeing chest pain every day for the rest of your career, and need a straightforward & systematic approach to these patients. The easiest approach is to divide them into 2 or 3 risk categories. Two category system = discharge or admission. Three category system = discharge, chest pain unit, or admission.

If you have a tremendous amount of clinical experience, categorization can be done by clinical gestalt. Otherwise, consider using a decision aid. The HEART score is one of many; expect "new & improved" CP decision aids in the future.



Article 1: Mahler SA, Hiestand BC, Goff DC et at. Can the HEART Score Safely Reduce Stress Testing and Cardiac Imaging in Patients at Low Risk for Major Adverse Cardiac Events? Crit Pathways in Cardiol. 2011;10:128-133.

In this study of registry data, 1070 low-risk ED chest pain patients defined as “low risk CP” by physician assessment and TIMI score < 2 were dichotomized into low vs. high risk “HEART” (History, ECG, Age, Risk factors, Troponin) score groups. Primary outcome was major adverse cardiac events (MACE = death, MI, revascularization) occurring by 30 days. MACE occurred in 0.6% patients with low risk HEART scores compared with 4.2% of patients with high risk scores (odds ratio 8, significant). High risk score was 58% sensitive and 85% specific for MACE. Authors also looked at adding serial troponins to the HEART score. Abnormal serial troponins + high risk HEART = 100% sensitivity to pick up MACE (95%CI 72-100%).

Author conclusion: in low risk chest pain patients, low HEART scores can be used to guide stress testing/cardiac imaging and significantly reduce cardiac testing.

Issues: These are already really low risk patients; only 1.1% of entire cohort had MACE. Low risk HEART score reduces MACE to 0.6%, eg you will still miss 0.5%. Unless you admit everyone, you’ll never get to zero misses. Important societal question concerns our acceptable miss rate. Important to include patient in discussion of risk stratification; personal “acceptable miss rate” will vary among patients. Logistical issues; retrospective registry trial, and 30% of patients were lost to follow-up.

Although serial troponins weren’t part of initial study design, only 2 patients with negative serial troponins had MACE; one went to CABG and the other had sudden cardiac death; could argue that neither of these are true “misses”. Reaffirms importance of serial troponins.

An important caveat about this study: it looked at patients already stratified as low risk, THEN applied the HEART score to help predict MACE and decide who needs stress/cardiac imaging. It was NOT a study of all-comers to an ED who present with chest pain. Authors think of the HEART score like PERC; to be used for additional risk stratification in low risk patients. Finally, this doesn’t address the question of who needs a troponin (low risk vs. no risk).

Bottom line: HEART score useful for new clinicians to help further risk stratify low risk CP patients and decrease ordering of stress tests. Experienced clinicians will likely use gestalt + 2 troponins to reach the same conclusions.

Additional Harwood comments: HEART score of 0-3 = less than 1% chance of MACE with 2 year F/U. HEART score of 0-3 along with a second negative troponin = MACE of 0%. Although it has not been validated prospectively, a heart score of 0 or 1, seems to be safe for discharge with a single negative troponin. HEART score of 4-6 = death/MI risk of 12% in 2 years. These patients would be a candidate for a chest pain unit protocol that accepts intermediate risk patients. HEART score of 7-10 = 65% chance of death/MI (Backus: 2010). Obviously, these patients generally are admitted and will often end up in the cath lab.


Article 2: Ely S, Chandra A, Mani G et al. Utility of Observation Units for Young Emergency Department Chest Pain Patients. JEM 2013;44:306-312.

This retrospective observational study evaluated outcomes of 239 patients ≤ 40 yr old enrolled in an ED observation unit due to suspected ACS. Enrollment required ECG without ST changes, negative trop, normal VS and no dysrhythmias. Primary outcome: to evaluate the rate of abnormal stress tests associated with significant CAD. Five patients had positive stress tests. One additional patient had troponin elevation and a negative cath, but was labeled as +MI. Stress testing identified one patient with intervenable ACS. There was an 80% false positive stress test rate. At one year followup, 2 MI and 1 PCI for overall adverse cardiac outcome rate of 0.8% (95% CI 0.1-2.5%). Author conclusion: observation and stress testing should not be routinely performed in this demographic unless other high-risk features are present.

Issues: didn’t consider cocaine, also didn’t identify why 1/3 of patients didn’t receive stress tests. Nine stress tests were “indeterminate”, without further testing or good followup. Overall lost to followup = 21%.

Bottom line: due to limitations/lack of followup, may not be practice changing, but reinforces results from other studies that stress testing in young CP patients has very low diagnostic utility, with high false positive stress test rates (leading to more unnecessary testing, cost, complications).


Article 3:Shah BN, Balaji G, Alhajiri A, et al. Incremental Diagnostic and Prognostic Value of Contemporary Stress Echocardiography in a Chest Pain Unit Mortality and Morbidity Outcomes From a Real-World Setting. Circ Cardiovasc Imaging. 2013;6:202-209.

Last and least. This retrospective study evaluated outcomes in 811 patients admitted to a chest pain unit with ≥ 2 cardiac risk factors and suspected ACS but nondiagnostic ECG and negative 12 hour troponin who received stress echocardiogram (SE) within 24 hours. Primary outcome was the accuracy of SE for predicting mortality/MI. At one year, 2% rate of death or MI; 0.5% of patients in normal SE vs. 6.6% of patients in abnormal SE group died or had MI. No difference in 30 day re-admission rates between normal/abnormal SE groups. Author conclusions: stress echos are awesome.

Interesting that these were not low risk patients (had cardiac risk factors). 50% of patients received ultrasound contrast agents (not typical practice). Excellent followup (97% followed up at least one year)

Harwood comment: Shah found if patient had normal SE, they had 0 deaths @ 6 month & about 1%/yr for the next 3 yrs. Remember, in Shah's study his pts with a (+) stress ECHO had a 16% death rate after 3 yrs. Mean age was 63 this was a sicker population that is seen in most USA CT angio studies. In Litt's study of 1400 pts, (NEJM 2012) mean age was 49. There were zero deaths @ 30 days.

Big question and fatal flaw: how does this study help us? As Erik stated, for any test, you want to know what information it provides above and beyond what we already know. No demographic information is provided in order to compare patients with abnormal and normal stress tests, and therefore we can’t know if the SE is providing any additional prognostic information. Erik contacted the senior author, who responded but stated that the requested information was not available. Hmmmm.

Additional Harwood comments:

--If the patient has a normal coronary CT angiogram, it appears as though the only a 1% chance of having a MACE the next 5 years. (see March journal club)

--Traditional teaching is that Stress ECHO has 15% False (+) rate & 15% False (-) rate. This is based on studies where all Pt's get Stress & caths (i.e., a very high pretest prob group of CP pts)

Rapid Blood Pressure Lowering in Patients with Acute Intracerebral Hemorrhage (INTERACT-2)

When a patient rolls in unresponsive and hypertensive intracranial hemorrhage is at the top of our differential. When the CT scan shows a large hemorrhage, we are quick to reverse coagulopathy if present, intubate if indicated, discuss the case with neurosurgery and pray. However, the management of blood pressure tends to vary based on the attending physician and their underlying training and experience. The dogma of avoiding blood pressure control because of concern over neurologic deterioration in acute intracerebral hemorrhage has been debated intensely.

Preliminary data had suggested that it reduced hematoma growth, a marker for poor outcomes in patients with ICH, but patient-oriented outcomes were lacking. A recent Study based on the original pilot study INTERACT1; INTERACT2 has just been published on May 29^th in the NEJM.

1.  Why is this topic important?

The current blood pressure management of patients with ICH is unknown. Guideline recommendations suggest maintaining a systolic blood pressure of <180 mmHg. However, many physicians still practice on old dogma that permissive hypertension be allowed to a systolic of < 180 and to avoid relative hypotension in order to maintain perfusion to the ischemic penumbra surrounding the hemorrhage.

2.  What does this study attempt to show?

This study attempts to demonstrate that in patients with spontaneous intracranial hemorrhage with:

1.   Hypertension, systolic BP > 180 mmHg

2.   Not early surgical candidates (who these people are no one knows)

3.   Had an admission GCS >5

4.    Did not have a large hematoma with a poor prognosis based on attending physician discretion

Were randomized to intensive blood pressure lowering to a systolic BP <140 within one hour of randomization and continuing with a goal blood pressure of <140 for the next 7 days or guideline therapy maintaining a systolic blood pressure below/near 180 mmHg.  The type of anti-hypertensive agent was not specified, and 7 main anti-hypertensive agents were used.

  The study attempts to demonstrate that in patients who receive early aggressive anti-hypertensive treatment, maintained for 7 days, there is improvement in death and disability, defined as a mRS >2.

3.  What are the essential findings?

A total of 2,839 participants were enrolled in the study, with > 60% of participants in each arm coming from China. 1,403 patients enrolled in the early intensive treatment arm, and 1,436 assigned to receive guideline-recommended treatment.

  Baseline characteristics were similar (NIHSS was slightly lower in the intensive treatment arm 10 vs. 11) Table 1.

  Also the hematoma volume (<15ml) and superficial location of the hematoma favored the treatment arm, (both known to be better prognostic markers) Figure 1.

   At 90 days 719 participants (52%) in the intensive-treatment group, as compared with 785 (55.6%) in the standard-treatment group, had a poor outcome defined as a mRS >2 (OR 0.87; 95% CI, 0.75-1.01; p = 0.06). Table 3.

   On ORDINAL analysis (different prespecified vantage point) there was a shift in the distribution of scores on the mRS favoring the intensive blood pressure-lowering treatment (OR 0.87; 95% CI, 0.77 to 1.00; P =0.04). Table 3.

   There was no difference in the pre-specified safety outcomes of ACS, hypotension, and neurologic deterioration in the first 24 hours, Table 3.

   An interesting finding was that there was no statistically significant decrease in size in hematoma expansion in the intensive lowering of blood pressure group at 24 hours, the presumed mechanism by which blood pressure management was thought to be protective.

4.  How is patient care impacted?

Given that there were few adverse events and that there is a small signal of potential benefit I can see the guidelines changing to recommend a more strict control of blood pressure after ICH. See below.

5.  Is this an area of controversy?

Acute management of blood pressure has been a critical question in all neurologic emergencies; stroke, subarachnoid hemorrhage and ICH. It is believed that auto-regulation of blood pressure by the cerebral vasculature is lost during neurologic insults such as ICH. The authors of the INTERACT2 trial believed the mechanism of benefit to be a reduced hematoma size, based on their pilot study INTERACT1. The trial failed to demonstrate this, but it must be mentioned that finding statistical significance among means may not be appropriate. There is potential that some patients had marked reduction in their hematoma size and they accounted for most of the benefit, but were washed out by the overwhelming number of patients who did not see such a reduction.

   Also it is possible that small reductions in hematoma volume (on the order of 2mL could have profound impact on neurologic sequelae, but this question remains unanswered.)

   It is also interesting that they picked a primary outcome of a mRS >2, because had they of picked a mRS of >1, as is typical in most acute stroke trials, the evidence of benefit would have been statistically significant with a lower end point (OR 0.83; 95% CI 0.70 to 0.98; p =0.03).

   This study although suggestive is certainly not definitive, and will be aided by the ATATCH2 study to be published in 2016. Proponents of blood-pressure control will argue that there is no downside to aggressive blood pressure control, and potential a benefit in an otherwise group of patients with a high morbidity and mortality rate. Others will argue that the baseline characteristics of the treatment arm were heavily favored, based on NIHSS, location of hemorrhage, and % of patients with initial hematoma volume < 15mL.

6.  Major Limitations of the study?

The study has several strengths. First it is a large multi-center randomized controlled trial. Their outcomes are patient-centric and they pre-specified their secondary outcomes and sub-group analysis.

   However, multiple flaws in the study design are present. First, the choice of anti-hypertensive agents was markedly different than is used primarily in the United States. Urapidil, a potent alpha antagonist was used in a third of patients in the intensive blood pressure control arm, and nicardipine and labetalol only accounted for another third. Other less titratable medications such as nitroprusside, furosemide, hydralazine and nitroglycerine accounted for the other third. This was almost certainly because 2/3’s of patients recruited in the study were from China. Whether or not this limits the generalizability of the results is questionable.

   In addition it is important to note that the results of ATATCH II (antihypertensive treatment of acute cerebral hemorrhage) is almost completed with recruitment, and the results of the study will be much anticipated in 2016. The study design is in North America, with similar inclusion criteria to the INTERACT2 study, except that nicardipine was used as the sole agent, and patients had to receive intensive blood pressure control in < 4 hours, whereas in the INTERACT2 trial 50% of patients were randomized after 4 hours.

Despite the limitations several an important concept was addressed:

 Intensive blood pressure control may have a neurologic benefit in patients with intracranial hemorrhage and at worst does not seem to result in any increased morbidity. The mechanism by which this occurs is not entirely clear.

Until next time!

-Dave

Anderson et al. Rapid Blood-Pressure Lowering in patients with Acute Intracerebral Hemorrhage. NEJM. 2013; 1-11. 

7 y/o

7/ o m presents to the ED after coughing while playing with legos. He is satting 100% on room air, comfortbale playing in the room. His CXR shows:

"There is no acute cardiopulmonary process. there is no evidence for

radiopaque foreign body. There is no significant evidence for air-trapping."

Decubitus films:

No evidence for air-trapping

We take a look at the CXR ourselves, do you see anything pecuilar? (CLICK ON XRAY its a thumbnail)

Look at the right mainstem area, can you make out the pinholes of a lego piece? Apparently there is no air trapping because the lego was not solid but had a hole in the middle of it!

It helps that he had unilateal wheezing on that side and stridor, but either way a piece of lego was removed form his right mainstem bronchus.

-dave

Pre-Hospital Intubation after Cardiac Arrest

Prehospital Advanced Airway Management with Neurologic Outcome and Survival in Patients with Out-Of-Hospital Cardiac Arrest

Out of Hospital Cardiac Arrest occurs in approximately 375-390K individuals yearly in the United States. Few interventions have ever been demonstrated to improve neurologically intact survival, and airway has always remained a priority in the initial resuscitation of the patients with cardiac arrest.

 Despite this, advanced airway management in patients with cardiac arrest has never been shown to improve mortality. In fact, several studies have challenged the commonly held belief that advanced airway management in the pre-hospital setting improves mortality in trauma patients and pediatric patients.

 In January JAMA published a prospective population based study completed in Japan looking at neurologically intact survival in patients who had pre-hospital advanced airway management (endotracheal intubation, or supraglottic airways) in a large cohort of patients.

 1.                Why is this topic important?

 Pre-hospital advanced airway management has long been a part of many EMS protocols, despite the lack of evidence for improved neurologic survival. This study evaluates a large cohort of patients with pre-hospital cardiac arrest and attempts to evaluate the effect on mortality and neurologic function at one month using a modified rankin scale (mRS) in patients who have advanced airway management vs. bag-valve mask ventilation.

 2.             What does this study attempt to show?

 The authors of the study believed that pre-hospital advanced airway management had no affect on neurologically intact survival.  They defined their outcomes as return of spontaneous circulation (ROSC), one-month survival and neurologically intact survival at one month (mRS >/= 2). The authors chose a set of potential confounders a priori based on biological plausibility and a priori knowledge. Age, sex, cause of cardiac arrest, first documented rhythm, witnessed arrest, type of bystander CPR, use of public AED, epinephrine administration, and time interval from call to CPR by EMS and from receipt of call to hospital arrival were all chosen.

 The authors recognized that a randomized controlled trial large enough to demonstrate clinical and statistical significance would be difficult due to the dismal outcome of cardiac arrest in general, and the large number of patients needed to show a meaningful difference. Instead they chose a population based study, completed prospectively acknowledging that potential confounders could have a significant impact on outcome.

 3.             What are the essential findings?

 A total of 649,359 patients were ultimately included (658,829 eligible), 367,837 (56.7%) underwent bag valve mask ventilation, and 281,522 underwent advanced airway management (43.5%).

 Of the patients who underwent advanced airway management a total of 41,972 (6.5%) received endotracheal intubation, and 239,550 received supraglottic airways (36.9%).

 Table 1 shows the demographics of patients with out of hospital cardiac arrest.

 Table 2 summarizes the survival outcomes, first unadjusted, adjusted for selected variables, and adjusted for all covariates.

 An overview is provided for ease here:

 Rates of ROSC:                                 

Unadjusted:

-BVM 25, 904 (7%)

-Endotracheal Intubation 3,514 (8.4%)

-Supraglottic Airway 12,785 (5.3%).

OR (95% CI) vs. Bag-Valve Mask adjusted for pre-specified variables:

-Endotracheal Intubation 0.86 (0.82-0.89)

-Supraglottic Airway 0.64 (0.62-0.65)

One-month Survival:

Unadjusted:

-BVM 19,643 (5.3%)

-Endotracheal Intubation 1,757 (4.2%)

-Supraglottic Airway 9,176 (3.8%)

OR (95% CI) vs. Bag-Valve Mask adjusted for pre-specified variables:

- Endotracheal intubation 0.72 (0.70-0.73)

- Supraglottic airway 0.71 (0.69-0.72)

Neurologically Favorable Survival (mRS >/= 2)

 Unadjusted:

- BVM 10,759 (2.9%)

- Endotracheal Intubation 432 (1%)

- Supraglottic Airway 2,724 (1.1%)

OR (95% CI) vs. Bag-Valve Mask adjusted for pre-specified variables:

- Endotracheal Intubation 0.41 (0.37-0.45)

- Supraglottic Airway 0.38 (0.36-0.40)

Plain Language summary-

 The unadjusted model demonstrated significant negative associations between ANY advanced airway management and the 3 end-point measures (P < 0.001 for all outcomes).

In the adjusted model using selected variables and all variables advanced airway management were independent negative predictors of all 3 outcomes (p < .0001).

 4. How is patient care impacted?

 This is a tough pill to swallow. I bet many people believe that this does not make much physiologic sense, how can providing oxygen to an apneic patient result in worse outcomes? Is it the additional time needed to secure the airway (if this were true why is the signal still present in patients receiving a LMA?), is it that patients who have an esophageal intubation are likely to die of asphyxiation? Is hyperoxia and reperfusion injury contributing to a significant portion of morbidity in the post-anoxic injured brain?

Or is the study really not able to account for all the variables, and a potential unidentified confounder was driving the increased morbidity and mortality rather than the advanced airway itself?

Maybe it is time to reassess the importance of advanced-airway management in patients with OOHCA, and instead focus on chest compression early recognition of ventricular fibrillation with defibrillation, and finding secondary causes of arrest (no intubation, and no epi/bicarb/atropine/pacing unless indicated). If the patient obtains ROSC then all bets are off.

5.  Is this an area of controversy?

There is really no point in stirring the pot with a mini-JC if there isn’t some type of controversy. Although some might argue that a true randomized clinical trial would be the only way to account for all differences in patients with OOHCA, I would argue that this is a large population based study. RCT’s are expensive, asses one intervention, apply only to a specific cohort of patients, and the OOHCA patients are a heterogenous group of patients. It is always difficult to account for every confounder, but in this study of almost six hundred thousand patients, there was a consistent signal of harm with pre-hospital intubation.

If this had completely gone against prior publications, it might raise a few more eyebrows, however, several studies have demonstrated that advanced airway management placed by pre-hospital providers does not improve and may worsen outcomes in patients with cardiac arrest.

6. Major Limitations of the study?

The study is non-randomized, and therefore most physicians argue that it cannot identify causation and only association. However, this is a large cohort study, the researchers identified a priori several possible confounders and attempted to adjust for these. The clinical end-point has been consistent in other smaller but more methodologically rigorous trials.

In addition they reran all the statistics favoring worse case scenarios in patients lost to follow-up and the signal of harm was still statistically and clinically significant.

Closing thoughts:

For me a 2% reduction in neurologically intact survival is important enough to have the discussion about changing pre-hospital management. Maybe one day we will learn that the drop in venous return, and subsequent hyperoxia from intubation was killing people. Whatever the truth may be the paper was worthy of a Mini-JC even if it might not change your practice tomorrow.

Till next time!

-Dave

Hasegawa et al. Association of Prehospital Advanced Airway Management With Neurologic Outcome and Survival in patients With Out-of-Hospital Cardiac Arrest. JAMA. 2013; 257-266.

Eastvold Pearl #26: SCIWORA

This is a long one.  But such an important topic.

The skinny on a case that I had.  80 yo M fell in front lawn while bending over to pick up sprinkler, fell forward striking head on ground (sounded like maybe from a foot or so) and then could not get up. Found by neighbor several hours later, and EMS called with transfer to ED.  Patient ambulatory on scene. Denies any pain or symptoms other than stating he felt weak.  My work-up in ED, negative CT head, EKG, troponin, CK, CXR, UA, and routine labs.  I did note that patient had a very difficult time rolling over in bed due to weakness.  Ambulated (known in the medical world as "leg stuff") without assistance or fall risk.  Recommended admission but the thought of nursing home placement kept this stoic Iowan out of the hospital...until he was brought back into the ED 12 hours later noting difficulty buttoning shirt and eating (known in the medical world as "arm stuff").  CT C-spine attained which was negative, admitted to hospital with MRI several days later revealing central cord syndrome.  Kind of sounds like a classic boards question in hindsight.  So, this was my 2nd SCIWORA case in 4 years.  Both patients injured their C-spines after falling from standing height.  So, what have I learned (apparently not enough yet)...see below.

Spinal cord injuries can be very subtle.  Why?  I think for 2 main reasons; crappy neuro exams and crappy knowledge of presenting symptoms. 

Pearl #1: Patients with spinal cord compression often do NOT have pain

.   My guy had zero neck pain or tenderness on exam.  We all tend to decide on the need to image the C-spine based on pain.  No pain or tenderness, squeeze my hands and wiggle your toes..C-collar off...usually you are okay with this approach.  However, you have to be really sure you are not missing subtle neurologic findings.

• Neurologic complaints without pain in the extremities are concerning for spinal cord compression. Neurologic complaints with neck pain and/or arm pain are concerning for cervical radiculopathy (i.e., compression on exiting dorsal root nerve)

• Obviously, neck pain is also concerning for potential fracture with osseous injuries leading to the most devastating injuries.  So the take home message is not that neck pain is benign, but the absence of neck pain does not exclude serious injury.

Pearl #2 - Neuro exam findings are often symmetrical

.  The cursory ED neuro exam misses these because we are so trained on detecting asymmetries, i.e., "brain stuff" or strokes.

• Motor complaints: Bilateral symmetrical weakness (or spasticity) concerning for spinal cord compression.   Unilateral weakness suggests radiculopathy.  To detect these deficits, you must test all joints that flex or extend, which will effectively test both proximal and distal motor function.

Pearl #3 - Sensory deficits are vague and NOT dermatomal

• Sensory complaints: vague bilateral non-dermatomal or multiple dermatomes involved is concerning for spinal cord compression.  Sharp demarcation or dermatomal loss is concerning for radiculopathy.

Pearl #4 - Test reflexes

• Bilateral reflex abnormalities, positive Hoffman's sign, and positive Babinski's sign are concerning for spinal cord compression

• Slight retraction of lower extremities when testing Babinski does not equal volitional movement.  I made this mistake in the intoxicated patient.  Very well documented false positive so to speak.

Pearl #5 - Autonomic complaints are always concerning for cord compression

: 

• Impotence or priaprism.  Remember the saying, if they are raising theirs you should raise your eyebrows...maybe that was for Bells palsy

• Bladder or bowel dysfunction

• Horners syndrome

Pearl #6 - The "Eastvold Washcloth Test" = Pain and temperature run together via the spinothalamic tract (anterior cord)

• Testing only pinprick can be [a] difficult to pick up on subtle deficits given as we all know this test is so subjective, "feels a little duller", [b] people malinger

• Easier and probably much more sensitive (based on my own anecdotal evidence) method is to test temperature with a cold wet washcloth.  Everyone wins, you will pick up on subtle deficits and the patient gets a sponge bath, which is hopefully their last as opposed to a sponge bath from the nurse at neuro rehab.

• If abnormality detected, then I test pinprick

Pearl #7 - Be Weary of Anyone with a Hyperextension Mechanism of Injury

• Both patients fell from standing height.  1st guy hit forehead on table with large laceration over forehead.  2nd guy had very small abrasion on chin, that's it.  Both are hyperextension injuries, and the most common subtype of SCIWORA.

• "Commonly observed in the spondylotic spine in association with low-energy mechanisms, such as fall from standing height, although it can be observed in younger patients in association with higher-energy mechanisms and acute disc herniations.  Clinically these patients often present with minor abrasions or lacerations on the scalp/forehead and a variable degree of neuologic impairment..."  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989526/

Pearl #8 - Fractured (aka broken, Gromis) Osteophytes on CT scan May Not Be Insignificant = Cervical spondylosis is a potential red flag

• Does not equal unstable C-spine injury, true

• Insignificant, false.  

• You will read that isolated osteophyte fractures are insignificant.  They are not unstable, but they may represent soft radiographic evidence of serious underlying ligamentous disruption

• How?  Due to spinal cord compression between a hypertrophied spondylotic disc-osteophyte complex and bulging ligamentum flavum

• Occurs with hyperextension (as well as hyperflexion) injuries.  There was likely considerable translational movement within the 3 spinal columns and ligamentous disruption at the time of injury, but with muscle spasm and return to normal alignment of the neck this disruption can be very subtle.  See Fig 7 below illustrating this important point.  I have seen this exact case.  Notice how well-aligned the spinal column is.

• > 80% of adult SCIWORA patients have underlying cervical spondylosis.  I feel pretty good about a negative MDCT scan with recons and no underlying spondylosis...and no neuro complaints.  If spondylosis is present, all patients with subjective or objective neuro findings need an MRI before clearing C-spine (and read pearl #7).  Further, I do a really thorough neuro exam (after my 2nd missed case) on patients with spondylosis without neuro complaints before clearing these patients.

• Lastly, EMRAP has officially failed on this topic (dammit Mel) spouting comments that if the CT C-spine is negative the chance of surgical intervention is zero.  Almost true, as the majority of these SCIWORA cases are managed conservatively.  I do agree that the overwhelming majority of patients with negative MDCT with recons and no subjective or objective neurologic findings do not need an MRI.  Patients with persistent severe neck pain is a judgment call, and if unsure you should involve your consultants.  Just be really careful about diagnosing someone with hysterical paralysis.

Pearl #9 - Patients with acute cervical spine injuries need interrogation of entire spine

• I need to do a better job of this

• If there is any C-spine injury, the patient needs at least CT of TLS spine and likely MRI

Pearl #10 - If you are doing plain films or flex-ex films, please just stop it

Feedback always welcome.

Next topic is how to manage compression fractures, this one has always bugged me with the lack of recommendations.

Josh

Workup for SAH

Journal Club Synopsis: Subarachnoid Hemorrhage (SAH): Do We Still Need the LP?

Thanks to Lisa and Ted Toerne for hosting and for the ridiculous Smoque BBQ, and to presenters Lindsay, Beau, Natalie, Pikul, J Cash, and Brian for their thoughtful critiques.

Background: Headache is the chief complaint for 3% of ED visits. Mixed in with all the benign headaches are 3-4% of patients with headache + normal neuro exam who have serious pathology. One elusive serious diagnosis is the “sentinel bleed” of SAH. Traditional teaching states that a negative CT is not definitive, and debates rage on about how many hundreds of LPs we perform to identify a sentinel SAH. We do plenty of other high volume low yield tests in order to identify rare but life threatening disease (may I have another ECG please), but even putting aside the discomfort and time requirements of LP, there are potential downsides (post LP headache, the rare spinal hematoma/abscess, and the risk of false positive “bloody taps” leading to further unnecessary testing). With the publication of the Perry article in 2011, the question was raised yet again: when considering SAH, is current CT technology finally sensitive enough to obviate the need for LP after a negative CT?

Article #1: Presenters: Lindsay Purnell, Beau Willison
Cortnum, Søren MD, et al: Determining the Sensitivity of Computed Tomography Scanning
in Early Detection of Subarachnoid Hemorrhage. Neurosurgery: May 2010 - Volume 66 -Issue 5 - p 900–905.

In this Danish retrospective study, medical records were reviewed from 499 patients referred to a neurosurgical unit due to suspicion of/confirmed SAH. All patients with a negative CT had a LP performed. Of 296 patients diagnosed with SAH, 295 were diagnosed on CT, and one was diagnosed on day 6 due to a positive LP. Post-LP headache rate was 7.4%. Of patients receiving LPs, 2% were diagnosed with viral meningitis. Authors concluded that CT had a sensitivity of 99.7% (95% CI 98.1-99.99%).

Sounds good. Unfortunately, their methods were horrible. A positive or negative LP was not defined, although they imply that they relied on xanthochromia. They also didn’t define their gold standard for the diagnosis of SAH. It’s unknown who was responsible for reading the CT scans (neurosurgeons ran the study, and did see the scans, but unknown if they were blinded to the study, and if they used an explicit data abstraction form…doubt it). There’s nothing about followup.

Also, there is the issue of referral bias. These are by definition sicker patients than our population, as they were referred to a neurosurgical center, and 60% were diagnosed with SAH. There is an unknown denominator of possible patients who could have been included, and young, healthy patients with bad headaches may not all get referred. Another way to think of it is in terms of spectrum bias, where a test performs differently in different patient populations. CT sensitivity is likely lower in less sick patients.

Bottom line: not practice changing due to poor methods and the referral/spectrum bias. Remember 2% of patients who received LP were diagnosed with viral meningitis-you may identify something besides blood.

Article #2: Presenters: Natalie Kmetuk, Pikul Patel
Jeffrey J Perry, Ian G Stiell, et al: Sensitivity of computed tomography performed within six
hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort
study BMJ 2011;343:d4277.

In this prospective study conducted in 11 tertiary care EDs across Canada, sensitivity of head CT for the diagnosis of SAH was evaluated in 3132 consecutively enrolled neurologically intact adult patients presenting with new acute HA peaking within one hour of onset. SAH rate was 7.7%. Sensitivity of CT for SAH was 92% (95% CI 89-95.5%), with a specificity of 100% (trying to identify specificity is silly here due to incorporation bias-if you define a “positive” using a test you’re evaluating, it has to be 100% specific). The reason this paper has received so much attention is that for the 953 patients receiving CT within 6 hours of HA onset, CT sensitivity was 100% (95% CI 97-100%). All patients were scanned on third generation multi-slice scanners.

Limitations: Only half the patients received LP after negative CT, and the adequacy of follow-up has been questioned. One patient ultimately diagnosed with SAH who had CT within 6 hours of HA onset was sent home after CT was read as negative by the ED physician and a radiology trainee. Additionally, 2292 potentially eligible patients were not enrolled. External validity questioned-will this hold up outside of academic centers?

Bottom line: This article offers support for CT without LP when considering SAH, if CT is performed on a modern scanner within 6 hours of HA onset, and is read by a qualified radiologist. That being said, there are nationally respected emergency physicians with widely divergent opinions on whether this study is enough to change practice.

Article #3: Presenters: Jennifer Cash, Brian Fort
Dustin G. Mark, MD, et al: Nontraumatic Subarachnoid Hemorrhage in the Setting of Negative Cranial Computed Tomography Results: External Validation of a Clinical and Imaging Prediction Rule. ePub2012 / Annals of Emergency Medicine 2012.

This study attempts external validation of a clinical decision instrument identifying high- risk clinical features for SAH in neurologically intact patients with headache. The derivation study was by Perry et al, and published in BMJ in 2010. In that article, they evaluated 1999 patients with max onset headache intensity within one hour (130 cases of SAH), and identified 3 combinations of history and exam findings that were 100% sensitive in identifying SAH. This study by Mark et al attempted to externally validate one of these instruments (investigate patients with any combination of age > 40, neck pain or stiffness, LOC, or HA onset during exertion), as well as the timing of imaging decision instrument described in article #2 (CT within 6 hours of HA onset) using a matched case-control study
of 55 patients over 11 years with normal neuro exam and diagnosis of SAH after (-) CT/ (+) LP. The combination of high-risk clinical features demonstrated a sensitivity of 97.1% (95% CI 88.6-99.7%), specificity of 22.7% (95% CI 16.6-29.8%), and a negative LR of 0.13 (95% CI 0.03-0.61) for the diagnosis of SAH. Twenty percent of SAH cases had negative CT results when performed within 6 hours of headache onset. The authors conclude that the high-risk clinical features may have some Bayesian utility, but that a 6 hour CT cut-off missed 20% of SAH.

Limitations: Retrospective case-control study design, with methodology that started with known SAH patients, rather than with patients presenting with undifferentiated headache. Also, someone was worried enough about these patients to push for an LP after negative CT; it’s not the same as in a prospective study where all patients with negative CT get LP, regardless of how persuasive the clinician was feeling that day.

Bottom line: External validation studies for decision instruments often report lower sensitivities than the initial derivation studies, especially when studies move from academic centers to the community. These decision instruments will need to be re- tested in a number of different practice settings before making definitive conclusions about their accuracy, but the high-risk clinical features may help determine pre/post test probabilities.

____________________________________________________________________________________________

Journal Club bottom line:

There was no consensus. Some in the room are ready to tell neurologically normal patients who are imaged for rule-out SAH within 6 hours of HA onset that if their CT is negative, they need no further evaluation. Others are not convinced, and given the high stakes of missing a sentinel bleed, will tell the same patient there is still up to a 1% of missed bleed (based on LRs, pre/post test probabilities-another discussion), and incorporate the patient’s risk tolerance into decisions about LP/further testing.

Certainly, these articles and the general discussion highlight the importance of “maximal intensity at onset” (within a few minutes) as the most important clinical feature of SAH, even more than “worst HA of life”. They also identify useful high risk clinical features (age > 40, LOC, neck pain or stiffness, HA onset during exertion, vomiting, SBP > 160, DBP > 100) that can help with pre/post test probabilities,
and impact which patients really need the hard sell for the LP after a negative CT, potentially even when CT is within 6 hours of HA onset. Final pearl-beware the patient who isn’t feeling better after analgesics and a negative CT-that’s another high-risk feature.

Endovascular Treatment for Acute Ischemic Stroke

 How many times have you spoken with interventional radiology and heard about the latest and greatest endovascular treatment for acute ischemic stroke? If they had their way, treatment for stroke will be treated just like STEMI and patients will be taken away to angiography suites. The physiology seems to make sense, remove the clot and improve perfusion, or does it? Up until now, evidence has come mostly from a “physicians experience”, non-randomized trials, or outcomes looking at revascularization rather than hard clinical end-points like neurologic function using a modified-rankin scale. The first, to my knowledge, of a published RCT comparing intravenous tPA vs. IA thrombolysis with threombectomy has been published in the NEJM.

1.  Why is this topic important?

Several non-randomized trials and cohort studies have suggested that thrombectomy and revascularization after acute ischemic stroke improves outcomes for patients with large vessel occlusions. Up until this point no randomized controlled trials comparing the current standard of care (IV tPA) with mechanical embolectomy has been undertaken. 

2.  What does this study attempt to show?

This study attempts to identify whether there is improved survival free of disability (defined as a modified Rankin score of 0 or 1 on a scale of 0 to 6 with 0 indicating no symptoms, 1 no clinically significant disability despite symptoms and 6 indicating death) at 3 months after acute ischemic stroke.

Patients were randomized within the 4.5-hour time frame if they had symptoms of a stroke and a head CT without signs of an ICH. Patients were randomized to one of two arms:

1. Intra-arterial thrombolysis with the option for mechanical thrombectomy.

2. Intravenous thrombolysis as previously described (NINDS and ECASS).

If patients were outside the time window of 4.5 hours they were excluded. Due to operator delays patients who were randomized to IA tPA could still receive treatment up to 6 hours as long as they were randomized prior to the 4.5 hour mark.

The interventionalist could instill up to 0.9 mg/kg (or 90mg) of IA tPA (the dose given IV) and not higher. They could use a mechanical device if the operator believed it was indicated. If upon angiography there was no identifiable thrombus the operator could instill tPA into the region that was presumably affected, if clinically warranted. If the patient had no neurologic deficit, or rapidly improving symptoms then the operator did not have to proceed with angiography.

3.  What are the essential findings?

Between February 1, 2008 and April 16^th 2012, 362 patients were enrolled. 181 patients in the IA +/- thrombectomy arm, and 181 in the IV tPA (control) arm. Baseline characteristics were similar (table 1). Average NIHSS was 13.

Of the 181 patients assigned to endovascular therapy, 15 did not receive the treatment (6 because of clinical improvement, 3 because of a lack of evidence of occlusion on angiography, 3 because of dissection, 1 because of an unknown bleeding diathesis, 1 because of a groin hematoma, 1 because of delayed availability of the interventionalist.) 3 procedures were interrupted due to equipment complications.

In total 165 patients underwent endovascular treatment. 109 had IA thrombolysis, and 56 had a device deployed. The median dose of tPA was 40mg.

Primary outcome at 90 days is show in figure 1. 30.4% of patients undergoing thrombectomy survived without disability, and 34.8% of patients in the IV tPA group survived without disability, OR 0.82 (95% CI 0.53-1.27; P=0.37).

At 90 days 26 patients in the endovascular treatment group (14.4%) and 18 in the intravenous (9.9%) group had died.

On secondary analysis, stratifying for time to randomization, age, NIHSS, stroke territory did not affect odds ratio as NONE favored the endovascular treatment. Overall treatment with IV tPA was favored (figure 2).

4.  How is patient care impacted?

In patients with acute ischemic stroke, this study represents the first relatively large randomized controlled trial comparing thrombectomy to intravenous tPA. IV tPA is cheaper, less labor intensive and appears to have similar and possibly improved efficacy compared with endovascular therapy. The trial does not support the routine use of interventional procedures for acute ischemic stroke.

Previously the consensus was that endovascular therapy was superior to IV tPA alone due to increased recanalization rates seen in previous trials. This theory made clinical sense, improve flow and save the ischemic penumbra. However, several studies just released in the NEJM refute this contention.

5.  Is this an area of controversy?

As always it is. The interventionalists will argue that t IV tPA can be followed by endovascular therapies for patients who do not achieve recanalization. Also, “the latest and greatest” retrieval devices will be argued to improve outcomes as these older devices were more “rudimentary.”

This study also does not even question the utility of tPA in acute ischemic stroke as apparently that bus has left the station, despite many randomized trials demonstrating harm.  Although I don’t think it is quite dead yet, Endovascular therapy may be added to the same bin as many other interventions before it: Vioxx, Xigris, Avandia, Diehtylstilbestrol…

6.  Major Limitations of the study?

The study is a well completed randomized controlled trial. However, several limitations still exist.

First, there were inconsistencies in what types of interventions were performed. Several patients randomized to the interventional arm got both IA tPA and thrombectomy while others received IA tPA alone. Also, the dosing of IA tPA was also not standardized, and this could potential confound the results. The authors acknowledge this when they state this is a pragmatic trial as there is no standard of IA tPA or when to deploy a mechanical device, as this is mostly based on operator experience.

In addition, it is possible that patients with angiography defined acute ischemic stroke in a large vessels may have greater benefit, as that was not part of the inclusion criteria in this trial. Only 1/3 of patients had a large vessel atherosclerosis or cardiogenic embolism as the cause (the rest were small-vessel and other). Therefore whether or not more benefit would be derived from obtaining a CTA and identifying these patients first is questionable. The authors argue that the CTA adds significant time delays to an already time sensitive situation and that the probability that a CTA adds significant benefit is “unlikely”.

Lastly some interventionalists ask for systemic thrombolysis first, and then complete thrombectomy afterwards. Whether this approach is more efficacious can not be ascertained by this study.

Take home points!

1.    Intra-arterial thrombolysis in acute ischemic stroke without systemic thrombolysis does not offer improved neurologic survival compared to systemic thrombolysis for acute ischemic stroke.

OF note several trials were all presented on Feburary 8^th 2013 at the international stroke conference, ALL WERE NEGATIVE. Abstracts provided below.

MR RESCUE- Kidwell and colleagues completed a randomized controlled trial in 118 patients within 8 hours after the onset of large-vessel, anterior-circulation strokes comparing mechanical embolectomy (Merci Retriever or Penumbra System) or receive standard care. Revascularization in the embolectomy group was achieved in 67% of the patients. Ninety-day mortality was 21%, and the rate of symptomatic intracranial hemorrhage was 4%; neither rate differed across groups. Among all patients, mean scores on the modified Rankin scale did not differ between embolectomy and standard care (3.9 vs. 3.9, P=0.99). Embolectomy was not superior to standard care in patients with either a favorable penumbral pattern (mean score, 3.9 vs. 3.4; P=0.23) or a nonpenumbral pattern (mean score, 4.0 vs. 4.4; P=0.32). In the primary analysis of scores on the 90-day modified Rankin scale, there was no interaction between the pretreatment imaging pattern and treatment assignment (P=0.14). Conclusion: A favorable penumbral pattern on neuroimaging did not identify patients who would differentially benefit from endovascular therapy for acute ischemic stroke, nor was embolectomy shown to be superior to standard care.

IMS III trial- In patients with moderate-to-severe acute ischemic stroke who received intravenous t-PA within 3 hours after symptom onset, Broderick et al randomly assigned eligible patients to receive additional endovascular therapy or not, in a 2:1 ratio. The study was stopped early because of futility after 656 participants had undergone randomization. The proportion of participants with a modified Rankin score of 2 or less (indicating functional independence) at 90 days did not differ significantly according to treatment (40.8% with endovascular therapy and 38.7% with intravenous t-PA alone; absolute adjusted difference, 1.5 % points; 95% CI 6.1 to 9.1). Mortality was unchanged at 90 days ( endovascular-therapy: 19.1% versus intravenous t-PA 21.6%; P=0.52), as was the proportion of patients with symptomatic intracerebral hemorrhage within 30 hours after initiation of t-PA (6.2% and 5.9%, respectively; P=0.83). Also, there were there no significant differences for the predefined subgroups of patients with an NIHSS score of >20 or <20. Conclusion: Additional endovascular therapy after intravenous t-PA was not associated with improved outcomes in acute ischaemic stroke.

Ciccone et al. Endovascular treatment for Acute Ischemic Stroke. NEJM. 2013; 1-10. 

UNTIL NEXT TIME!

-Dave

Blood Transfusions in UGI Bleeding

TRANSFUSIONS IN ACUTE UPPER GASTROINTESTINAL BLEEDING

Transfusion thresholds in medicine have been steadily falling, as more and more literature demonstrates either no improvement in outcomes or associated harms.  

Today’s mini-JC focuses on a topic extremely relevant to our practice as emergency physicians: transfusion thresholds of PRBC’s in patients with acute upper gastrointestinal bleeding (UGIB). If the patient is exsanguinating, we all know what to do, but what about in hemodynamically stable patients with an upper GI bleed?

1.  Why is this topic important?

Several non-randomized trials, and animals studies have evaluated a restrictive approach to blood transfusion in patients with bleeding from portal hypertension, as increases in effective circulating volume may lead to a rebound in portal pressure, which is associated with a risk of re-bleeding.

In addition, trauma surgery has propagated the idea of “don’t pop the clot” in patients who have penetrating trauma in order to prevent rebleeding and coagulopathy after surgery. These same mechanisms have been suggested to be beneficial in patients with arterial hemorrhage from a perforated peptic ulcer.

2.  What does this study attempt to show?

This study attempts to demonstrate that in patients with UGIB without massive exsanguination, a restrictive transfusion threshold of 7 is non-inferior to a transfusion threshold of 9. Patients were eligible if they had hematemesis, (or bloody nasogastric aspirate), melena or both as confirmed by hospital staff.

They attempted to exclude critically ill patients as well as completely stable patients as defined below:

-Patients were excluded if they had a lower GI bleed, active acute coronary syndrome (new EKG findings or positive biomarkers), massive exsanguination (hypotension, with active bleeding requiring emergent transfusion), or acute CVA.

-Patients with rockall score of 0, or a hemoglobin of 12 or greater were also excluded as these patients represented the lowest risk group.

Patients were randomized to a restrictive (transfuse if hgb <7, goal hgb 7-9) or liberal (transfuse if hgb <9, goal 9-11) transfusion groups. Randomization also was stratified for presence or absence of cirrhosis in blocks of four.

Treatment was otherwise kept the same between the two groups (protonix bolus and drip, emergency EGD within 6 hours with banding or sclerotherapy as necessary, octreotide and antibiotics if the bleed was deemed to be variceal.)

3.  What are the essential findings?

A total of 921 patients underwent randomization and 32 were withdrawn or withdrawn by investigators. 444 patients were left in the restrictive-strategy group and 445 in the liberal-transfusion group. Baseline characteristics were similar in both groups, as described in table 1.

225 (51%) of patients in the liberal group got transfusions, as compared with 61 (14%) in the restrictive group.

Mortality at 45 days was significantly lower in the restrictive-strategy group than in the liberal group 5% (23 patients) as compared with 9% (41 patients) hazard ratio 0.55 (0.33-0.92) respectively, p < 0.05.  

Death was due to unsuccessfully controlled bleeding in 3 patients in the restrictive strategy group (0.7%), and 14 patients in the liberal strategy group (3.1%).

Overall the liberal strategy group got more blood, had more rebleeding and thus required more salvage procedures especially in patients with variceal bleeding (TIPS and balloon tamponade). There were more medical associated deaths (sepsis, acute MI, acute CVA etc.) in patients who received the liberal transfusion strategies.  

4.  How is patient care impacted?

Among patients with severe acute upper gastrointestinal hemorrhage a restrictive strategy of blood transfusion improved mortality at 45 days. This survival benefit was likely conferred due to better control of factors contributing to death, such as further bleeding, rescue therapy and adverse events.  

5.  Is this an area of controversy?

Although this is an area of controversy, the evidence that blood transfusions, especially older blood in which the oxygen carrying capacity has diminished, may result in increased complications has been suggested previously. The TRICC trial, the Houston study, and several other large randomized controlled trials have all shown that patients have improved or equivalent outcomes when using a restrictive transfusion strategy.  The mechanisms for this difference in mortality are certainly different, as we know that transfusions may propagate further bleeding in patients at risk of hemorrhage. In addition, it is known that blood transfusions can result in significant immunomodulation and cytokine release resulting in acute renal failure, pulmonary edema, ARDS, and higher infectious complications in the critically ill medical patient.

This must be balanced in the situation in which acute hemorrhage is life threatening and rapid transfusion is required to restore the effective circulating blood volume.  

6.  Major Limitations of the study?

The study is a well completed randomized controlled trial. However, several limitations still exist. First, there is no direct statement as to what was defined as a life-threatening hemorrhage that excluded patients from the trial, and therefore knowing how to apply this to our patients is somewhat confusing. In addition, 32 patients were withdrawn from the study because the investigator did not believe that there was clinical equipoise. They do not further specify this in the intention to treat analysis, and how many patients from each group were removed (if all 32 patients from the restrictive strategy group were removed because the attending physicians believed that they required blood transfusions this could have a significant effect on the statistically significant mortality benefit shown in this paper.)

However, despite some limitations in the study there are several important concepts:

1.    Transfusing patients based on hemoglobin levels only may be short sighted. Looking at perfusion parameters (lactate, oxygen delivery, end organ malperfusion) may be a more appropriate approach rather than transfusing to a number (MUST KEEP KGB > 9).  

2.    Giving a blood product should be viewed as giving a potentially dangerous medication (not dissimilar to heparin, Plavix etc.) and each time you order it you should consider the risks and the benefits. It has been demonstrated time and time again that blood products have associated harms (certainly I am not arguing against transfusing the actively bleeding patient with obvious signs of malperfusion), especially in the elderly patients with multiple comorbidities or patients with cancer.

UNTIL NEXT TIME

-Dave

Villanueva et al. Transfusions Strategies for Acute Upper gastrointestinal Bleeding. NEJM. 2013; 368:11-21.

62y/o AMS weakness, sob

62y/o M presents to the ED with AMS, bradycardia. We cannot get an IV but he looks liek S***. He is short of breath, DEXI is 42, no IV access, Im putting an IO since he is awake but clearly confused. We are trying to still get a full set of vitals and an EKG (since he was a code 44 at 540am). He is defintiely intubatable, but it looks like pulse ox is 100% on NRB, so we have a minute here. 

I am shooting a quick EKG while pushing an amp of D50 into the IO (which by the way, he didn't complain at all while putting in the IO, but he DID NOT like the D50 getting pushed in). 

Just then the EKG  tech says hey his EKG is looking really funny, just as the patient goes unresponsive:

EKG 1.

Not so good, 2 amps of calcium chloride, 2 amps of bicarb, 30 seconds of CPR followed by intubation with rocuronium (he was still breathing.)

EKG 2:

Potassium came back 8.0, acute renal failure, got dialysis a few hours later and despite our best efforts died in the MICCU. Hyperkalemia is scary, but treatable, first and foremost diagnosis in ANYONE with bradycarida without P waves should be hyperK. 

Eastvold Pearl #25: Anterior MI w/o reciprocal cahnge

As we reflect on the year 2012, it is important to know what does not "reflect" (corny stretch) in the world of EKGs.  Fifty percent of anterior STEMIs lack reciprocal changes.  This is crazy but a fact.  I will try to summarize why this occurs, but you may want to read the attached article.  

We have all learned that reciprocal changes are important in diagnosing STEMIs, and their presence increases the likelihood that the EKG pattern is secondary to coronary occlusion.  Further this concept of reciprocal changes is the main focus of my "Swans Reflecting Elephants" talk, whereby localized ST depression is invariably secondary to subtle STEMIs.  

But does the absence of reciprocal change rule out MI?  The answer is no.  As stated above, 50% of anterior STEMIs lack reciprocal changes.  

That said,  inferior STEMIs will almost always have STD (albeit may be subtle) in I/AVL or at least new TWI in AVL.  Lateral STEMIs also will have reciprocal change.   

The pathophysiology of inferior ST segment changes in the setting of anterior STEMI is actually pretty cool.  I have read a lot on this, and I think you will like this article I am attaching.  To summarize, in the setting of anterior STEMIs there are 3 patterns of inferior ST segment changes, [a] ST depression, [b] ST elevation, and [c] No ST change.  Group "c" accounts for 50%, quoted many times in the literature.  

Look at Figures 1, 2, and 3 in the paper, as this is the best explanation on this issue that I have found.

-- Anterior STEMI with inferior ST depression occurs because the occlusion is proximal LAD (proximal to D1 or 1st diagonal), with infarction extending to high lateral wall.  Thus the inferior ST depression actually represents true reciprocal change from lateral ischemia.  Anterolateral STEMI.

-- Anterior STEMI with inferior ST elevation occurs the the occlusion is distal to D1 AND wrap-around LAD (a variant) that supplies the inferior wall, thus causing inferior STEMI.

-- Anterior STEMI with no inferior ST changes occur in 2 settings, which is exemplified in example #3 in the paper.  [1] Occlusion distal to D1 with no wrap-around LAD, so no infarction of lateral (distal) or inferior (no wrap-around) regions.  There is NO reciprocal change for true anterior ischemia.   [2] This setting is the cool one.  If you have a proximal LAD lesion to D1 AND a wrap-around LAD, the ST changes counteract each other.

Josh

Eastvold Pearl #24: False Positive Lactate

Hey guys,

   Worked a shift at UIHC with a resident who got a lactate on a hemodynamically stable asthmatic, and it came back at 4.6.  Repeat arterial lactate similar.  If you practice drone medicine like this internal medicine resident was doing, you'll be heading down the wrong path ..."pretty much means we need to put a central line in, and I guess start antibiotics."

What the resident didn't know was that asthmatic patients on continuous albuterol nebs will have a type B lactic acidemia.  Although the mechanism is not completely understood, β2-agonists are known to stimulate cyclic adenosine monophosphate (cAMP)-mediated glycogenolysis and lipolysis.  Hyperglycemia and free fatty acid inhibition of pyruvate dehydrogenase lead to anaerobic metabolism of pyruvate to lactate, thus causing elevated lactate levels.  Work of breathing has also been hypothesized to contribute as well.

There are many other causes of type B lactic acidemias, just google them.

Eastvold Pearl #23: Swollen Scrotum

Hey guys,

  I have been absent for a while, and hope to send more of these out.  This one was provoked by the conference notes sent (great idea btw).  I ran across a patient with a non-infectious complication from peritoneal dialysis...the massively swollen scrotum.  

65 yo M with h/o ESRD on CAPD presented to ED with [1] massively swollen scrotum (his concern), and honestly [2] facial droop (wife's concern) for 5 days, which turned out to be a Bells palsy or peripheral CN VII palsy.  You gotta love a guy like this.

We have all seen massive scrotal edema in the setting of anasarca, with the work-up really having nothing to do with GU but merely a work-up for anasarca.  

What was different with this guy was that he had no lower extremity or abdominal wall edema, it was all isolated to his scrotum and penis.  No hernia on exam or bedside US.

Quick google search at work, popping out the attached article, then pretending I knew this beforehand as I talked to the nephrologist on-call really changed the work-up and treatment for this patient. 

It turns out that patient with continuous ambulatory peritoneal dialysis (CAPD) have about a 5% risk of dialysate leakage, representing a non-infectious complication of CAPD that we should know.  Why is this important, these patients will need to stop PD and switch to hemodialysis as part of the treatment.  Thus, they will need to be admitted as most do not have HD capabilities.  Why to have to stop PD?  See below and read attached article if time.

PD dialysate leaks are classified as early (1st 30 days of catheter placement) or late (>30 days).  The above complication is a late complication, which is what I'll cover.  Late leaks most often "related to mechanical or surgical tear in the peritoneal membrane, presenting as internal leakage (e.g., pleural cavity, abdominal wall, external genitalia).  Enhanced stress on the supporting abdominal wall structure may lead to" leakage and/or hernia.  The leakage can be considered a mechanical intra-abdominal pressure-related complication due to micro-tears (which may seal up with cessation of PD) or larger tears or hernias (which require surgery).

Diagnosis: Known in the nephrology field as "skinny legs, big scrotum."  May need US to rule out hernia, or CT with PD catheter-instilled contrast to evaluate for leakage based on extravasation of contrast outside peritoneal cavity.

Treatment: [1] Stop CAPD for 1-3 weeks, again this will require most to be admitted. [2] Switch to temporary hemodialysis, which is thought to allow these micro-tears to seal up. [3] Surgery if recurrence after re-initiating CAPD.  Other indications for surgery are concurrent hernia, and some advocate that genital edema is an indication for surgery as these patients fail the PD rest period.

Josh

Reference:  Dialysate Leaks in Peritoneal Dialysis. Semin Dial. 2001 Jan-Feb;14(1):50-4. Leblanc M, Ouimet D, Pichette V. Nephrology Division, Maisonneuve-Rosemont Hospital, University of Montreal, Quebec, Canada.

Dialysate leakage represents a major noninfectious complication of peritoneal dialysis (PD). An exit-site leak refers to the appearance of any moisture around the PD catheter identified as dialysate; however, the spectrum of dialysate leaks also includes any dialysate loss from the peritoneal cavity other than via the lumen of the catheter. The incidence of dialysate leakage is somewhat more than 5% in continuous ambulatory peritoneal dialysis (CAPD) patients, but this percentage probably underestimates the number of early leaks. The incidence of hydrothorax or pleural leak as a complication of PD remains unclear. Factors identified as potentially related to dialysate leakage are those related to the technique of PD catheter insertion, the way PD is initiated, and weakness of the abdominal wall. The pediatric literature tends to favor Tenckhoff catheters over other catheters as being superior with respect to dialysate leakage, but no consensus on catheter choice exists for adults in this regard. An association has been found between early leaks (< or =30 days) and immediate CAPD initiation and perhaps median catheter insertion. Risk factors contributing to abdominal weakness appear to predispose mostly to late leaks; one or more of them can generally be identified in the majority of patients. Early leakage most often manifests as a pericatheter leak. Late leaks may present more subtly with subcutaneous swelling and edema, weight gain, peripheral or genital edema, and apparent ultrafiltration failure. Dyspnea is the first clinical clue to the diagnosis of a pleural leak. Late leaks tend to develop during the first year of CAPD. The most widely used approach to determine the exact site of the leakage is with computed tomography after infusion of 2 L of dialysis fluid containing radiocontrast material. Treatments for dialysate leaks include surgical repair, temporary transfer to hemodialysis, lower dialysate volumes, and PD with a cycler. Recent recommendation propose a standard approach to the treatment of early and late dialysate leaks: 1-2 weeks of rest from CAPD, and surgery if recurrence. Surgical repair has been strongly suggested for leakage causing genital swelling. Delaying CAPD for 14 days after catheter insertion may prevent early leakage. Initiating CAPD with low dialysate volume has also been recommended as a good practice measure. Although peritonitis and exit-site infections are the most frequent causes of technical failure in peritoneal dialysis (PD), dialysate leaks represent one of the major noninfectious complications of PD. In some instances, dialysate leakage may lead to discontinuation of the technique (1). Despite its importance, the incidence, risk factors, management, and outcome of dialysate leakage are poorly characterized in the literature. We will review the limited available information on this topic in the next few sections. PMID: 11208040 [PubMed - indexed for MEDLINE]

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