Episode 23 – SBO and Mesenteric Ischemia

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The Free Open Access Medical Education (FOAM)

This week we’re covering Dr. Jacob Avila’s post on ultrasound for small bowel obstruction (SBO)  located at Ultrasound of the week.  He has an accompanying video on 5minSono.

Point of care ultrasound has good operating characteristics for diagnosis of SBO with a LR+ 9.5, LR- 0.04, far better than abdominal x-ray [1].

Screen Shot 2015-01-25 at 10.20.44 AM

What to look for:

  • Dilated loops of bowel > 2.5 cm in diameter
  • Additional clues:  “To and fro” peristalsis
  • The piano key sign, Tanga sign
Piano Key Sign

Piano Key Sign

Problems with abdominal x-ray:

  • Rosen’s: Abdominal x-rays are “diagnostic in approximately 50 to 60% of cases of SBO, equivocal in 20 to 30%, and normal, nonspecific, or misleading in 10 to 20%” [2].
  • American College of Radiology: they can “prolong the evaluation period … while often not obviating the need for additional examinations, particularly CT” [3].

Limitations:

  • While ultrasound can diagnose SBO, there is little evidence to suggest that we can identify transition points or strangulation/necrosis.  As such, there can still be a role for CT scan, particularly in first time SBO to identify a transition point.
  • The EAST guidelines acknowledge the utility of ultrasound yet this practice is far from accepted in the surgical community.  Surgical colleagues will likely still want concrete imaging such as an x-ray or CT; however, ultrasound performed concurrent with the history and physical may speed up patient’s disposition to definitive care/imaging.
Possible algorithm for use of US in SBO

Possible algorithm for use of US in SBO

More FOAM on the topic:

The Bread and Butter

We cover key points on SBO and Acute Mesenteric Ischemia from Rosenalli, that’s Tintinalli (7e) Chapter 86; Rosen’s (8e) Chapter 92.  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Small Bowel Obstruction

Etiology of intestinal obstruction: “HANG IV.” Hernia, Adhesions (most common cause), Neoplasm, Gallstone ileus, Intussusception, Volvulus

Treatment

  • Intravenous fluids – resuscitate the patient!
  • Antiemetics.  If a patient is compromising their airway, an aspiration risk, or vomiting despite antiemetics, consider the use of a nasogastric tube.  Shockingly, “use of nasogastric decompression is considered dogma by many emergency physicians and surgeons, its effect in decreasing the duration of SBO has scant support in the medical literature” [2, 5].  This point demonstrates that SBO is not a monolithic disease entity but a spectrum of pathology with variable treatments depending on patient’s sickness.
  • Antibiotics that cover gram-negative and anaerobic organisms
  • Admit. Most of these patients will likely go to the surgical service; however,

Acute Mesenteric Ischemia

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 Generously Donated Rosh Review Questions (scroll for answers)

Question 1. A 73-year-old man presents with vomiting and abdominal pain for 2 days. The patient has a remote history of cholecystectomy and appendectomy. Examination reveals a markedly distended abdomen and absent bowel sounds. Lab studies show an elevated WBC count and a lactate of 4.3 mmol/L. An abdominal radiograph is obtained that is shown below. 

Screen Shot 2015-01-26 at 8.40.19 AM

Question 2. An 87-year-old woman presents with worsening abdominal pain over the last 24 hours. She has minimal tenderness on examination but an elevated lactic acid. An abdominal CT Scan demonstrates mesenteric ischemia.

References:

1. Taylor MR, Lalani N. Adult small bowel obstruction. Acad Emerg Med. 2013;20(6):528–44.

2. Roline CE, Reardon RF.  “Disorders of the Small Intestine.  Rosen’s Emergency Medicine.  8th ed. pp 1216-1224.e2.

3. Ros PR, Huprich JE. ACR Appropriateness Criteria on suspected small-bowel obstruction. J Am Coll Radiol. 2006;3:(11)838-41.

4. Vicario SJ, Price TG.  “Bowel Obstruction and Volvulus.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide.  7th ed. pp 581-583.

5.  Fonseca AL, Schuster KM, Maung AA, Kaplan LJ, Davis KA. Routine nasogastric decompression in small bowel obstruction: is it really necessary? Am Surg. 2013;79:(4)422-8.

Answers.

1. D. This patient presents with a high-grade small bowel obstruction (SBO) with evidence of bowel ischemia (elevated lactate). Mortality has fallen in the last century with aggressive surgical treatment (from 60% to 5%). The abdominal radiograph above shows multiple air-fluid levels consistent with an SBO. Radiographs are abnormal in 50-60% of cases and are more likely to demonstrate abnormality when the obstruction is high-grade versus partial. Two views (upright and supine or supine and decubitus) should be obtained. Mechanical obstruction refers to the presence of a physical barrier to the flow of intestinal contents. In a simple obstruction, the intestinal lumen is partially or completely obstructed causing intestinal distension proximally but does not cause compromise of the vascular supply. In a closed-loop obstruction, a segment of bowel is obstructed at two sequential sites usually by twisting on a hernia opening or adhesive band leading to compromise of blood flow eventually resulting in bowel ischemia. Ischemia may only be seen on CT scan or occasionally, on laparoscopy or laparotomy. However, an elevated lactate in the setting of an SBO is highly suggestive of intestinal ischemia. The presence of blood in stool (either gross blood or guaiac positive stools) also suggests the presence of ischemia or infarction. When compromise of the vascular supply is suspected, the patient should have an emergent surgical consultation for operative management. Immediate management should also include placement of a nasogastric tube for decompression of the proximal parts of the intestines, intravascular volume resuscitation and intravenous antibiotics when vascular compromise is suspected or confirmed. CT scan of the abdomen and pelvis (A) is considered complimentary to plain films and is more sensitive and specific. Additionally, CT scan can reveal the site and cause of obstruction. However, surgical evaluation of a high-grade SBO should not be delayed for advanced imaging. Colonoscopy (B) is not indicated in small bowel obstruction. There is an increased risk of perforation. An enema and polyethylene glycol (C) is the treatment for constipation, and may worsen the outcome in patients with high-grade bowel obstruction.

2. Arterial emboli account for more than 50% of cases of mesenteric ischemia. The classic presentation of mesenteric ischemia is abdominal pain out of proportion to examination. Most commonly, thrombi develop in the left ventricle or atrium and embolize into the aorta. From the aorta, the emboli pass into one of the branches supplying the circulation to the gut. Thesuperior mesenteric artery is the most common site of embolization because of its large diameter and narrow angle of takeoff from the aorta. Mesenteric ischemia usually involves the small intestine and sometimes the right colon. The large intestine has significantly more collateral flow and is not as susceptible to ischemia. Aortic dissection (A) may lead to mesenteric ischemia depending on the location of the dissection. It is also possible to have a primary dissection of the mesenteric blood supply (e.g. SMA).Primary arterial thrombosis (C) of the mesentery is much less common and arises from progression of underlying atherosclerotic disease. Patients will often have a history of intestinal “angina” or chronic mesenteric ischemia during which symptoms occur after eating when the gut requires additional blood supply which is limited by the atherosclerotic changes. Venous thrombosis (D) is the least common etiology of mesenteric ischemia and most commonly affects the superior mesenteric vein.

FOAMcastini – Reflections on ACEP tPA Clinical Policy Update Draft

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As detailed in this FOAMcastini, ACEP just released a draft of an updated clinical policy on tPA for acute ischemic stroke.  This came in the wake of years of controversy over the aggressive position taken in the 2012 clinical policy.

While FOAMcast is not an interview style podcast, we felt compelled to get some perspective on Emergency Physicians a little more experienced than ourselves.  Here we interview:

Dr. Ryan Radecki (@emlitofnote), Assistant Professor, University of Texas – Houston

  • We don’t know who best benefits from tPA so elucidating which patients are “carefully selected” may get hard.
  • See his response to the policy on his blog here

Dr. David Newman (#draftnewman), Associate Professor of Emergency Medicine, Mount Sinai Hospital

  • The process for ACEP clinical policy creation seems to work.  The constituency expressed concern and the college listened and went back and re-created the policy from the bottom up.
  • This policy reflects a move from content expert to methodologists which better reflects the evidence compared with opinions (and is the standard per USPSTF).

Dr. Anand Swaminathan (@EMSwami), Assistant Professor of Emergency Medicine, NYU

  • Inclusion of more rigorous methodology and review of evidence.
  • May be perceived as too “soft” by tPA supporters.  This policy may not overtly change practice but may open up avenue of conversations.

Dr. Ken Milne (@thesgem), Chief of Staff at South Huron Hospital

  • When looking at “carefully selected” patients, as noted in the policy, remember to use the Evidence Based Medicine trifecta of evidence, patient values, and clinical expertise.  In isolation, one component is not sufficient.
  • Previous discussions of NINDS, and the Cochrane tPA article

FOAMcastini – ACEP tPA Clinical Policy Update

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The Free Open Access Medical Education (FOAM)

Comment on the 2015 ACEP tPA Clinical Policy Draft here

ACEP tPA Clinical Policy 2012 – This policy has been entrenched in controversy since it was published.  Why?  Well, largely because the evidence was given a stronger level recommendation than the data supported, conflicts of interest abounded, and the data (mostly from NINDS (The SGEM review), ECASS, and IST-3) were problematic.  This has been well covered by these reviews of the clinical policy:

What changed in the 2015 draft?

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Episode 22 – The Knee

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This week we’re covering a post from the incredible pediatric resource, Don’t Forget the Bubbles, “Knee X-ray Interpretation” by Dr. Tessa Davis.  We use a systematic approach to assessing chest x-rays, so why not knee x-rays?

  •  Know the anatomy
  •  Look at:
    • Effusion
    • Main bones
    • Tibiofemoral alignment
    • Tibial plateaus
    • Intercondylar eminence
    • Patellar tendon disruption
    • Patellar fracture

The Bread and Butter

We summarize some key topics from Rosenalli, that’s Tintinalli (7e) Chapter s271, 281; Rosen’s (8e) Chapters 57, 136.  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Knee Dislocation

  • Anterior is most common (40%), posterior (33%)
  • Approximately 50% of knee dislocations may be relocated upon presentation to the hospital (this does not reduce risk of badness)
  • Most worrisome sequelae = popliteal artery disruption.  Of patients with popliteal disruption, the amputation rate rises to 90% 8 hours after the injury without surgical intervention.
  • Workup may depend on your institution (ex: angiogram vs. CT angio vs. ultrasound) but all patients will need an ABI + 24 hour of pulse checks per current standards.
Screen Shot 2015-01-08 at 1.10.48 PM

Algorithm (adopted from Rosen’s)

Septic Arthritis

  • Most Common Organisms: S. aureus, N. gonorrhea
  • Hematogenous spread
  • Most Common Location: knee, hip

Risk factors such as immunocompromised hosts and use of steroids are risk factors for septic arthritis but the ones with the highest likelihood ratio (LR+ >10 is ideal):

  • Skin infection overlying prosthetic joint (LR+ 15)
  • Joint surgery within the preceding 3 months (LR+ 6.9)
  • Age > 80 (LR+ 3.5)

Diagnosis:  In the red, hot, swollen, painful joint, think septic arthritis.  Clinical and laboratory indicators aren’t great. Synovial fluid analysis, particularly the culture exists as the gold standard.  Arthrocentesis Trick of the Trade from ALiEM. Here are the operating characteristics from Margaretten et al:

  • Fever: Sensitivity 57%
  • Lab tests: White Blood Cell count (WBC), sedimentation rate (ESR), and c-reactive protein don’t perform well
    • WBC LR+  1.4 (1.1-1.8); LR- 0.28 (0.07-1.10)
    • Erythrocyte sedimentation rate 1.3 (1.1-1.8); LR- 0.17 (0.20-1.30)
    • C-reactive protein  1.6 (1.1-2.5); LR- 0.44 (0.24-0.82)
  • Synovial fluid gram stain and culture is the “gold standard.”

Treatment: Intravenous antibiotics and washout of the joint by orthopedics in the operating room

 Generously Donated Rosh Review Questions 

Question 1. A 67-year-old man with a history of gout presents with atraumatic left knee pain. Physical examination reveals an effusion with overlying warmth and erythema. There is pain with passive range of motion. He reports a history of gout in this joint in the past. 

Question 2.  A 27-year-old woman presents with severe left knee pain after an MVC where she was the front passenger. She states her knee hit the dashboard. An X-ray of the patient’s knee is shown below. After reduction, the physical examination reveals swelling of the knee and an Ankle-Brachial Index (ABI) of 0.8. 

Screen Shot 2015-01-12 at 5.13.06 PM

Answers.

1. D. Septic arthritis is a bacterial or fungal infection of a joint typically spread hematogenously unless there is direct bacterial contamination. The synovium is highly vascular and lacks a basement membrane making it susceptible to bacterial seeding. Certain conditions predispose individuals to septic arthritis including diabetes, sickle cell disease, immunocompromise, alcoholism or pre-existing joint disease like rheumatoid arthritis or gout. Fever is present in less than half of cases of septic arthritis so with clinical suspicion an arthrocentesis is indicated. The knee is the most common joint affected and patients have pain (especially on passive range of motion) and decreased range of motion often accompanied by warmth, erythema and fever. This patient may have an acute gouty flare, but the clinician must exclude an infection. On joint fluid analysis, the white blood cell count of a septic joint is typically > 50,000. Indomethacin (B) is a non-steroidal anti-inflammatory agent commonly used in the treatment of acute gout. Gout is an arthritis caused by deposition of monosodium urate monohydrate crystals in the joint space. Acute flares involve a monoarticular arthritis with a red, hot, swollen and tender joint. Acute episodes of gout result from overproduction or decreased secretion of uric acid. However, measurement of serum uric acid (C) does not correlate with the presence of absence of an acute flare. A radiograph of the knee (D) may show chronic degenerative changes associated with gout but will not help to differentiate a gouty arthritis versus septic arthritis.

2. C. Obtain Angiography. This patient presents with a knee dislocation and signs of a popliteal artery injury requiring angiography for diagnosis. A knee dislocation refers to a dislocation of the tibia in relation to the femur and not a patellofemoral dislocation. A tibiofemoral dislocation is a limb-threatening emergency due to the high rate of popliteal artery injury. The neurovascular bundle (popliteal artery, popliteal vein and common peroneal nerve) runs posteriorly in the popliteal fossa. The popliteal artery is tethered to the femur and tibia by a fibrous tunnel and is inherently immobile making it susceptible to injury during dislocation. Knee dislocations typically occur in major trauma. An MVC where the knee strikes the dashboard is a common scenario. The dislocation is usually clinically obvious and should be emergently reduced regardless of the presence of confirmatory X-rays. The leg should rapidly be assessed for any “hard” signs of vascular injury including an absence of pulse, limb ischemia, rapidly expanding hematoma, the presence of a bruit or thrill and pulsatile bleeding. Neurologic status should also be assessed prior to and after reduction. After reduction, all patients should have ankle-brachial index (ABI) performed. A normal ABI is > 0.9. Any patient with an ABI less than this should be further investigated for a popliteal injury with angiography. Splint and elevation (D) may be appropriate once a vascular injury is ruled out. The patient should not be discharged home (A) with an abnormal ABI. Observation and repeat ABI (B) is indicated if the initial ABI is normal.

Episode 21 – Acute Kidney Injury

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Dr. Josh Farkas of the PulmCrit blog has produced a couple of blog posts on the importance of renal protection in sepsis, Renoresuscitation: Sepsis resuscitation designed to avoid long-term complications and Renal microvascular hemodynamics in sepsis: a new paradigm.  Much of this is theoretical and certainly not something that is standard practice, rathery a theory extrapolated from subgroups of several trials.

Suggested renoresuscitation measures:

(1) Avoid renal failure – avoid nephrotoxins (many antibiotics, NSAIDs, ace-inhibitors), avoid hyperchloremic metabolic acidosis.

(2) Avoid volume overload – treating decreased urine output by flooding a patient with fluids is not necessarily the best move.

(3) Protect the glycocalyx of the endothelium – this suggestion proffers more questions than answers. Steroids? Albumin? Certain vasopressors?  Stay tuned, as we’re not really certain what this entails.

The Bread and Butter

We summarize some key topics from Rosenalli, that’s Tintinalli (7e) Chapter 91; Rosen’s (8e) Chapter 97.  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Acute Kidney Injury – typically a creatinine 1.5-2x the patient’s baseline is classified as acute kidney injury.  Urine output can be increased initially but determine whether a patient is making urine and how much, as urine output <0.5 mL/kg/h qualifies as AKI.

RIFLE criteria

RIFLE criteria

Importance – AKI is associated with worse outcomes, although it’s unclear as to whether this is merely a marker of

  • Found in 35-65% of admissions to the intensive care unit, in 5-20% of hospital admissions.  Furthermore, AKI is associated with higher mortality.
  • Renal failure can also cause significant problems for the patient such as electrolyte abnormalities (hyperkalemia the most worriesome, but also hyperphosphatemia) and pulmonary edema.

Etiology - many causes of AKI are reversible or amenable to treatment.

Prerenal – this is one of the most common causes of acute kidney injury and basically is caused by decreased blood flow to the kidney.  Associated with a high BUN/creatinine ratio, increased urine osmolality, a urine sodium concentration less than 20 mEq/L, and FENa less than 1% (this is why getting urine sodium and a concurrent chemistry panel is key).

  • Hypovolemia – volume depleted, hemorrhage, intravascular volume depletion from congestive heart failure or cirrhosis.
  • Hypotension – poor cardiac output (heart failure, valvular problems), shock
  • Decreased flow through the renal artery disease – Nonsteroidal anti-inflammatories: inhibit prostaglandins in the afferent arteriole.  ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, leading to decreased levels of angiotensin II, which when absent decreases the GFR because of dilatation of the efferent arteriole.

Post Renal (Obstructive) – Check out Episode 2 on urologic emergencies.

  • Benign prostatic hypertrophy (BPH) is the most common cause but medications such as anticholinergics and pseudoephedrine. Trauma, stones, strictures, and malignancy can also cause obstruction.

Intrinsic acute renal failure- divided into: tubular disease (most common), glomerular disease, vascular disease and interstitial disease.

  • Least common form of AKI in the ED, more common in inpatients.
  • Acute Tubular Necrosis (ATN) most common cause – via nephrotoxins such as aminoglycosides and contrast.
  • Granular “muddy brown” casts – think of necrosis from the “N” in ATN and necrosis tends to be dark.

Indications for emergent dialysis – AEIOU

A- Acidosis

E- Electrolyte emergencies (hyperkalemia!)

I-  Intoxication with dialyzable toxins (ethylene glycol)

O- Overloaded with volume

U- Uremia

 Generously Donated Rosh Review Questions 

Question 1. A 72-year-old man is brought to the ED from a nursing home for evaluation of oliguria. He is found to have an acutely elevated BUN and plasma creatinine from baseline. A Foley catheter is placed; his urine sodium (UNa) is measured below 20 mEq/L and fractional excretion of sodium (FENa) below 1%. 

Question 2.  A 54-year-old man presents to the ED in acute renal failure (ARF).

Answer 1.  D. This patient’s oliguria with acutely elevated BUN and plasma creatinine suggest that he is in acute renal failure (ARF). His UNa <20 mEq/L and FENa <1% indicate that he has intact reabsorptive function and is able to conserve sodium. This is consistent with prerenal azotemia as the cause for his ARF.

Acute tubular necrosis (ATN) (A), loop diuretics (e.g., furosemide) (B), and osmotic diuresis (e.g., mannitol) (C)all lead to UNa >20 mEq/L and FENa >1% because there is impairment in the ability to concentrate the urine. In such cases, a high-sodium load is excreted.

Answer 2. A.   Acute tubular necrosis (ATN) is a severe form of impairment of tubular epithelial cells caused by ischemia or toxic injury. It is a leading cause of ARF. One of its hallmarks is the presence of brown granular casts on urinalysis. These contain cellular debris rich in cytochrome pigments. In contrast, hyaline casts (B) are usually nonspecific but present after exercise; red cell casts (C) are indicative of glomerular hematuria (e.g., glomerulonephritis); and white cell casts (D) imply renal parenchymal inflammation (e.g., acute interstitial nephritis, pyelonephritis).

Episode 20 – Anticoagulation

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The Free Open Access Medical Education (FOAM)

We review Dr. Rory Spiegel’s, A Case of Identity Part Two, post on EMNerd which is essentially a take down of dual antiplatelet therapy (DAT) in acute coronary syndrome (ACS).  The bottom line?  There’s no demonstrable and clinically significant benefit from DAT as demonstrated in the trials below.

CURE trial – composite endpoints of questionable clinical significance and an enormous sample size.

  • 2.1% absolute decrease in cardiovascular death and myocardial infarction (MI), completely powered by the 1.5% absolute difference in MIs. Almost all of these MIs were Type IV and peri-procedural. Mortality between groups was identical at 30 days and end of follow up (1.0% vs 1.1% and 2.3% vs 2.4%, respectively).

ACCOAST – RCT of prasugrel or placebo prior to angiography

  • No difference in cardiovascular death, myocardial infarct, stroke, urgent revascularization or glycoprotein IIb/IIIa rescue therapy (10.8% vs 10.8%)
  • Approximately 1% increase in major bleeding

CREDO – RCT with placebo or clopidogrel 3-24 hours prior to urgent cardiac catheterization

  • No statistical difference  in the rates of death, stroke or MI at 28 days
  • Statistical significance of a secondary endpoint of the 1-year outcomes with a 2% absolute reduction in the rate of death, MI, and stroke, largely the result of a 1.9% reduction of MIs.
  • 1% increase in major bleeding events

Thienopyridine Meta-Analysis

  • In patients with non-ST elevation ACS, pretreatment with thienopyridines is not associated with reduced mortality but comes at a cost of a significant excess of major bleeding.

Composite endpoints are problematic (see this post, “Would You Rather“) and statistical significance claimed in these trials is largely a product of composite outcomes rather than patient oriented measures.

The Bread and Butter

We summarize some key topics from the following readings, Goldfrank (10th ed) Chapter 60, EMPractice October 2013 (there’s almost nothing in Rosenalli on this topic) but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Aspirin

  • Irreversibly inhibits platelets (for the duration of platelet’s life)

Ibuprofen

  • Reversibly inhibits platelets

Novel Oral Anticoagulants (NOACs)

NOACs have gained increased popularity and are slowly supplanting warfarin for common anticoagulation indications such as non-valvular atrial fibrillation (NVAF) as well as treatment of venous thromboembolisms such as pulmonary embolism (PE) and deep venous thrombosis (DVT).

Direct thrombin inhibitor - dabigatran (Pradaxa).  This drug was the first to supplant warfarin for NVAF in the United States, billed as more patient friendly given the lack of purported need for routine monitoring.  Recent investigations by Cohen et al, however, demonstrate that monitoring may, in fact, be safer.  Further, in a real world, retrospective cohort of Medicare beneficiaries given either dabigatran or warfarin for atrial fibrillation, major bleeding of the dabigatran cohort was higher than in the warfarin cohort 9.0% (95% CI 7.8 – 10.2) versus 5.9% (95% CI 5.1 – 6.6) after propensity matching [Hernandez].  For more on the problems with dabigatran, check out Emergency Medicine Literature of Note.

  • Predominantly renal excretion
    • Caution with impaired renal function (can cause dabigatran to stick around longer)
    • Hemodialysis an option in acute overdose; however, most people would probably not want to put a dialysis catheter in a coagulopathic patient.
  • Half-life ~ 15 hours
  • Can elevate the PTT. If the PTT is normal, likely not coagulopathic secondary to dabigatran [Dager et al].
  • No reversal agent

Factor XA inhibitors – these have XA in the name….rivaroXAban, apiXAban, edoXAban.

Rivaroxaban – approved for NVAF and treatment of DVT/PE.  Half life approximately 6-9 hours.

Apixaban – approved for NVAF and treatment of DVT/PE. Half life about 12 hours.

Edoxaban – approved for NVAF. Half life about 10-14 hours.

Bleeding Duration from ACCP

Bleeding Duration from ACCP

  • Cleared by liver and kidneys.
  • Can elevate the prothrombin time (PT), but not reliably. Specific assays exist but are not widely available and are expensive.
  • No specific reversal agent although andexanet alfa is in the pipeline.  It’s a Factor Xa decoy (Andexanet Alfa) that binds up the F10A inhibitors like a sponge. Read more here.
  • In the setting of major bleeding, guidelines recommend 4 factor PCCs.  A recent study demonstrates reduction in bleeding using 4 factor PCCs on healthy patients given edoxaban [Zahir et al, EMLitofNote].  The benefit of 4 factor PCCs is predominantly based on improvement in numbers, not patient oriented benefit and is discussed in these posts by Dr. Spiegel The Sign of Four, The Sign of Four Part 2.

More FOAM on Anticoagulation Reversal

Generously Donated Rosh Review Questions 

Question 1. A 65-year-old man with a metal aortic valve presents with hematemesis. His vitals are BP 95/50 and HR 118. The patient is on warfarin and has an INR of 7.3. 

Question 2. A 66-year-old woman with atrial fibrillation on warfarin presents with dark stools for 2 days. Her vitals are T 37.7°C, HR 136, BP 81/43, RR 24, and oxygen saturation 94%. Her labs reveal a hematocrit of 19.4% (baseline 33.1%) and an INR of 6.1. 

 

Answers.

1. D.  The patient presents with life-threatening bleeding and an elevated INR from warfarin use requiring immediate anticoagulant reversal regardless of the indication for anticoagulation. Warfarin acts by inhibiting vitamin K recycling thus limiting the effectiveness of vitamin K dependant clotting factors (factors II, VII, IX and X). The effect of warfarin can be measured using the prothrombin time or the INR. Warfarin is indicated for anticoagulation for a number of disorders including the presence of a metal valve. Patients with metal valves are at a higher 1-year risk of clot formation around the valve and subsequent embolic stroke. The therapeutic goal of warfarin in a patient with a metallic valve is usually between 2.5 –  3.5 or 3.0 – 4.0. Despite the increased stroke risk, patients with life-threatening bleeding should always have their warfarin reversed by administration of vitamin K and fresh frozen plasma (FFP). Alternatively, prothrombin complex concentrates can be given instead of FFP.

Warfarin is not amenable to hemodialysis (A) for removal or reversal. Although patients with a mechanical valve are at an increased stroke risk (increased 1 year risk) reversal should not be delayed (B), as the patient is more likely to die in the immediate situation from their gastrointestinal bleed. Platelet transfusion (C) will not help, as warfarin does not inhibit platelet function.

2. C.  The patient has a life-threatening gastrointestinal bleed in the setting of anticoagulation with warfarin, a vitamin K antagonist. Warfarin acts by inhibiting the synthesis of vitamin K-dependant factors in the coagulation cascade (II, VII, IX, X, protein C, and protein S). The anticoagulant effect of warfarin should be reversed as part of the patient’s emergent treatment. Fresh frozen plasma (FFP) contains all factors in the coagulation cascade and should be given in patients with major bleeding and elevated INR. Vitamin K should be given IV in critically ill patients with elevated INR because it shortens the time to effect.

Vitamin K should not be given intramuscularly (B) because absorption via this route is highly variable. Vitamin K should also not be given orally (D) in critically ill patients because the onset of action will be delayed. Additionally, absorption in patients with gastrointestinal bleeding may be variable. Vitamin K should be given along with FFP (A) because the factors inhibited rely on vitamin K for function.

Episode 19 – Environment: Mushrooms and Hypothermia

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The Free Open Access Medical Education (FOAM)

We review the Tox Talk podcast, Episode 23 – Mushrooms.  Our favorite pearls:

Clitocybe, Inocybe – contain muscarine which stimulates muscarinic receptors (acetylcholine/parasympathetic), causing a cholinergic toxidrome. Think SLUDGE (salivation, lacrimation, urination, defecation, gastric emptying/emesis) and the Killer B’s (bradycardia, bronchorrhea, bronchospasm) or DUMBELLS (diarrhea/diaphoresis, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation). Basically, cholinergic toxidrome: SMALL, WET, SLOW.

  • Memory aid: these mushrooms end in -yBE, akin to the “killer B’s” that make cholinergic toxicity deadly.

Gyromitra – (false morel) contains gyromitrin which can cause seizures, in addition to gastrointestinal upset and liver failure.  Treatment: pyridoxine (B6).

  • Memory aid: gyromitra named because they look like the gyri of the brain and, conveniently, make the brain seize through depletion of GABA.

Amanita phalloides – contains amatoxins which cause delayed gastrointestinal symptoms and liver failure., echoing acetaminophen toxicity.

  • Caution: this is different than the amanita muscaria ‘mushroom, which is tricky because that amanita muscaria has neither muscarinic properties nor the toxicity of amanita phalloides.

Bonus pearl: Coprinus species can cause a disulfiram like reaction.

FOAM article on mushrooms by Jo et al

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter  ; Rosen’s 8(e) Chapter  – but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Hypothermia starts at 35°C and then is categorized based on severity.

Pearls:

  • Ethanol + hypothermia = bad news.  Ethanol is the most common cause of excessive heat loss in urban areas as people tend to not take warming measures, may be homeless or without heat, and have impaired thermoregulation.  Hypothermia also slows alcohol metabolism, making people drunker for longer.
  • Elderly patients are more susceptible to hypothermia, particularly as they may not sense the cooler temperatures.  Some may also have impaired thermoregulation.
  • Have a low threshold

Diagnostics:

  • Get a temperature, on all patients.  This applies to patient’s “found down” as well as the chronic alcoholic who just seems really drunk.
  • If patients aren’t rewarming 1°C/hr and they’re above 32°C, consider: sepsis, cortisol deficiency, myxedema, ethanol.
  • The J wave or “Osborn” wave is found in many cases of hypothermia, often quoted at ~80%.  However, it is not pathognomonic for hypothermia.

From the Rosh Review

Treatment: Warm the patient.  Don’t call the patient dead until they’re warm and dead, which means their temp is above 30-32°C.

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Passive Rewarming - effective when the patient can still shiver (33-35°C).

  • Generates ~1.5°C of heat/hr

Active Rewarming - direct transfer of heat to the patient.

  • Indications: Cardiovascular instability, temp ≤30-32° C, inadequate rate of rewarming or failure to rewarm, endocrine problem, trauma, tox, secondary hypothermia impairing thermoregulation
  • Can be external or internal (which can be minimally invasive like IV fluids or quite invasive with things like bypass or pleural lavage).

Outcomes

  • Unlikely survival with a potassium > 12 mmol/L and recommendations are to terminate resuscitation for potassium >12 mmol/L and consider cessation for potassium between 10-12 mmol/L

FOAM Resources:

EBM Gone Wild on Prognostication

ScanCrit on ECMO in Accidental Hypothermia

EMCrit on Severe Accidental Hypothermia

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1.  A 40-year-old man with a history of substance abuse is brought in by EMS after being found unconscious outside of a nightclub in the middle of winter. It is unclear how long he was outside. He is unresponsive with a GCS of 3.

Question 2.  What is the most common cause of death in hypothermic patients after successful resuscitation?

Question 3.

Question 4. What abnormal rhythm is common with temperatures below 32°C?

References:

Danzl DF, Zafren K. Accidental Hypothermia, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2013, (Ch) 140: pp 1883-1885.

Brown D JA, Brugger H, et al. Accidental Hypothermia. N Engl J Med 2012;367:1930-1938.

Mair P, Kornberger E, et al. Prognostic markers in patients with severe accidental hypothermia and cardiocirculatory arrest. Resuscitation 1994;27:47-54.

Answers:

1. D. When the serum potassium is greater than 12 mmol/L resuscitative efforts should be halted as the patient is unlikely to survive and further efforts constitute futile care. Accidental hypothermia is not an uncommon occurrence particularly in colder climates. It may occur in conjunction with substance abuse when an individual becomes impaired and is subsequently exposed to the outdoors. It can also occur as a result of drowning, avalanche and other trauma. Bio-makers other than potassium have been studied including serum lactate (B), pH (C) and clotting time. None have been proven prognostically reliable and therefore should not be used as a guide to determine if resuscitation should be continued. Hypothermic patients that present in cardiac arrest should be warmed to a minimum of 32°C (A) preferably via ECMO or cardiopulmonary bypass. However, if a hypothermic patient is warmed to 32°C and remains in asystole, recovery is unlikely and resuscitative efforts should be terminated. Other indications to cease resuscitative efforts include: obvious signs of irreversible death (e.g. major trauma), valid DNR order, conditions that are unsafe for the rescuer or provider, and an avalanche burial > 35 minutes in which the airway is packed with snow and the patient is asystolic.

2. Pulmonary edema.

2. C. Hypothermia. The ECG demonstrates the presence of J waves or Osborn waves which are seen in hypothermia. One of the first cardiac effects of hypothermia is bradycardia secondary to decreased firing of the cardiac pacemaker cells in cold temperatures. Osborn waves may appear at any temperature below 32°C. The waves are an upward deflection at the terminal portion of the QRS complex. They may represent abnormal ion flux in cold temperatures along with delayed depolarization and early repolarization of the left ventricular wall. As temperatures continue to drop, the ECG will demonstrate prolonged intervals: PR, followed by QRS and then QTc. Both diabetic ketoacidosis (A) and digoxin toxicity (B) may lead to hyperkalemia. In diabetic ketoacidosis, hyperkalemia develops as a result of the acidic pH in the blood and the transport of hydrogen ions intracellularly in exchange for a potassium ion. Digoxin toxicity poisons the cellular Na+/K+ ATPase resulting in elevated extracellular levels of potassium. The ECG manifestations of hyperkalemia begin with peaked T waves. Multiple other findings eventually develop including a shortened QT interval, ST depression, bundle branch blocks, widened QRS, prolonged PR interval, flattened T wave and ultimately a sine wave. Hyperparathyroidism (D) may lead to hypercalcemia. In hypercalcemia, the ECG shows a shortened QT interval, flattened T waves and QRS widening at very high levels.

4.  Atrial fibrillation.