FOAMcastini – Kappa

(ITUNES OR LISTEN HERE)

Reading papers is hugely important but learning how to read medical literature is an entirely different realm and many of us have statsphobia.

The Free Open Access Medical Education (FOAM)

Kappa – It’s Greek To Me

The Bread and Butter

Kappa – a coefficient indicating the degree of inter-rater reliability.  How reliability are people getting the same result for a certain test or evaluation?

  • For example, you would want two people looking at the same chest x-ray to agree on the presence or absence of an infiltrate. Sometimes, chance comes into play and kappa tries to account for this.  Similarly, clinical decision aids are often comprised of various historical and physical features.  It would be nice if different clinicians evaluating the same patient would turn up the same results (thereby yielding the decision aid consistent and reliable).

To see how to calculate kappa, check this out.

The value of kappa ranges from -1 (perfect disagreement that is not due to chance) to +1 (perfect agreement that IS due to chance).  A value of 0 means than any agreement is entirely due to chance [1-2].

kappa

People debate over what a “good” kappa is.  Some say 0.6,  some say 0.5 [1-2]. In the PECARN decision aid, for example, the authors only included variables with a kappa of 0.5 [3-4].

Limitations:

  • Prevalence – if prevalence is high, chance agreement is also high.  Kappa takes into account the prevalence index; however, raters may also be predisposed to not diagnose a rare condition, so that the prevalence index provides only an indirect indication of true prevalence, altered by rater behavior [6].
  • The raters – agreement may vary based on rater skill, experience, or education.  For example, when PECARN variables were looked at between nurses and physicians, the overall kappa for “low risk” by PECARN was 0.32, below the acceptable threshold as this number suggests much of the agreement may be due to chance [6].
  • Kappa is based on the assumption that ratings are independent (ie a rater does not know the category assigned by a prior rater).

References
1. Viera AJ, Garrett JM. Understanding interobserver agreement: the kappa statistic. Fam Med. 2005;37:(5)360-3.

2. McGinn T, Wyer PC, Newman TB, et al. Tips for teachers of evidence-based medicine: 3. Understanding and calculating kappa. CMAJ. 2004;171 (11)

3.Kuppermann N, Holmes JF, Dayan PS, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374:(9696)1160-70. [pubmed]

4. Gorelick MH, Atabaki SM, Hoyle J, et al. Interobserver agreement in assessment of clinical variables in children with blunt head trauma. Acad Emerg Med. 2008;15:(9)812-8.

5. Nigrovic LE, Schonfeld D, Dayan PS, Fitz BM, Mitchell SR, Kuppermann N. Nurse and Physician Agreement in the Assessment of Minor Blunt Head Trauma. Pediatrics. 2013.

6. de Vet HC, Mokkink LB, Terwee CB, Hoekstra OS, Knol DL.  Clinicians are right not to like Cohen’s κ 2013;346:f2125

PlayPlay

Episode 24 – Mild Traumatic Brain Injury/Concussion

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

We cover the Taming the SRU podcast, “Ketamine Cagematch” (iTunes), a debate between Dr. Minh Le Cong and Dr. Chris Zammit.

Dogma persists that ketamine may increase intracranial pressure, which would be bad in traumatic brain injury (TBI) given the fixed space in the cranial vault.  These are largely from Yet, these patients often need sedation, for agitation or intubation, and drops in blood pressure are also deleterious (see EMCrit on neuroprotective intubation).

PRO (Le Cong): The literature doesn’t show clinically significant deleterious outcomes from ketamine use in the head injured patient.  Review in Annals on ketamine and ICP.  Deleterious effects of apnea may result from other sedative agents.

CON (Zammit): Studies showing that ketamine does not increase ICP confounded by the presence of other sedatives on board.  As a result, there may still be a risk to using ketamine in these patients.

The Bread and Butter

We cover key points on concussion and mild TBI from Tintinalli 254 but to be honest, Rosenalli is lacking on this topic so we’ve turned to the ACEP clinical policy, AAN guidelines, Ontario Pediatric Guidelines, and the  AAP guidelines on the topic.  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Mild TBI and concussion are often referred to interchangeably and the definition varies [1-3].  Unfortunately, concussion is often thought of only in the sports population and not all-comers to the Emergency Department (ED) so patients may not receive proper .

Definition: Essentially, any alteration in mental status following head injury. Per the CDC:  Head injury from blunt trauma or acceleration/deceleration with GCS 14-15 PLUS

  • observed or self-reported transient confusion, disorientation, or impaired consciousness
  • Amnesia around the time of injury
  • Signs of other neurologic or neuropsychological dysfunction
  • Any loss of consciousness (LOC) less than 30 minutes (!) [3]

For more on how reliable LOC is in these patients, see this post.

Causes: Falls and motor vehicle collisions are the most common causes in adults, whereas sports are the more common in kids.

  • The effects on the brain are largely a result of “secondary injury,” consistent of alterations in ion-channel, metabolic pathways, and electrochemical imbalances.  These are more functional than structural.

Symptoms: There’s a good bit of overlap with migraine, more significant head trauma, and symptoms that may be confused for behavioral issues in younger populations.

Screen Shot 2015-02-19 at 1.27.09 PM

Testing: Not all head injuries require imaging.  Certainly, patients with focal neurologic findings warrant imaging; yet, in other cases, validated decision aids exist to help determine which patients may or may not need imaging.  In adults, we like the Canadian CT Head tool , although the ACEP clinical policy uses the New Orleans Criteria.  For a solid review of the two, check out this SGEM episode.  In children, consider the use of the PECARN decision aid. Otherwise, a good neurologic exam and observation should suffice.

Something to consider – patients often believe that a “normal” CT scan of the head means that they don’t have a concussion.  As a result, they may not take concussion precautions seriously.  In this case, imaging may provide false reassurance.

There’s increased attention on biomarkers like GFAP, total tau, and S-100B but these are not ready for prime time and are not incredibly specific [3].  Further, standardized assessment tools such as SCAT3 and ACE may be useful, but are used predominantly on-site for sports related incidents.

Treatment

  • Education – this is one of the biggest areas in which ED providers may make a difference. Give patients or family members precautions for concussion, even if the injury or mechanism seems relatively mild.  Studies show that a majority of pediatric patients do not follow up as instructed after a concussion [4].  Perhaps communication of the the potential gravity of concussion and long-term implications may improve follow up.
  • Rest – This the is the mainstay of initial treatment for most mild TBI [1-3, 5].  It’s unclear how strict this rest needs to be, but a recent study in the pediatric literature found no benefit to strict rest versus standard instructions (1-2 days rest + graduated return) [6].
  • Graduated return to activity – after a period of rest, it’s recommended to slowly resume activities, spending at least 24 hours at each level of increased activity.  If an individual gets symptomatic, they should return to the level of activity at which they were asymptomatic (see the Zurich protocol).
  • Return to play – clearing people from the ED is NOT a good idea.  For those on the sidelines, a player should be removed from activity for the day after a suspected concussion.

Why do we care in the ED?

  • Quality of Life – Concussive symptoms can be quite disabling.  Giving patients a name for their symptoms, resources, and education may help them understand the process of recovery and available resources.
  • Second Impact Syndrome – A second head injury in a patient symptomatic from a concussion may experience diffuse cerebral edema, possibly from loss of cerebral autoregulation.* [2]
  • Post Concussion Syndrome (PCS) – a subset of the concussion population will have persistence of symptoms which, if they persist > 1 week to 3 months after the injury, is deemed PCS. *  This is thought to be more prevalent in individuals with a history of depression, anxiety, or migraines and in those with more severe ED presentations [2].
  • Bouncebacks – Patients may present to the ED with symptoms of concussion but may not give a history of significant trauma.  Remember that concussion may occur after a seemingly minor bump to the head and elderly may need extra support with activities of daily living or may bounce back with a more life threatening injury.
  • Lack of follow up.  While some may follow up with concussion specialists, the majority of our patient population lacks the ability for meaningful or specialist follow up.  We can’t assume that someone else is going to guide our patients through concussion recovery or that when we write “follow  up with _____” that it will happen.  Our care may be it, make it good.

*The literature on these is sparse and complicated by variable definitions, information, and standardized reporting.

 Generously Donated Rosh Review Questions (scroll for answers)

Question 1. A 33-year-old man with no past medical history presents with a headache 3 days after a closed head injury. The patient states that he stood up from kneeling and hit the top of his head on a wood cabinet. There was no loss of consciousness or seizure activity. In addition to the headache, he complains of difficulty concentrating at work and dizziness. His physical examination is unremarkable.[polldaddy poll=8663736]

Question 2. A 42-year-old man is brought to the ED after he tripped and fell while he and his wife were on a walk. His wife notes that she saw him hit his head on the pavement and that he did not respond to her for 45 seconds. When he started to respond, she says that he was very confused. In the ED, his vital signs are BP 135/75, HR 88, RR 14, and oxygen saturation 98% on room air. On exam, you note some minor lacerations on the patient’s upper extremities, face, and scalp and his GCS is 15. As the wife recounts what happened, the patient does not recall any of the events and continuously asks to repeat what happened to him. A CT scan of the brain is normal. The patient is diagnosed with a concussion and is ready to be discharged from the ED. [polldaddy poll=8663741]

References

1. Tavender EJ, Bosch M, Green S, et al. Quality and consistency of guidelines for the management of mild traumatic brain injury in the emergency department. Acad Emerg Med. 2011;18:(8)880-9. [pubmed]

2. Haydel M.  Management Of Mild Traumatic Brain Injury In The Emergency Department. Emergency Medicine Practice.  September 2012 Volume 14, Number 9

3. Jagoda AS, Bazarian JJ, Bruns JJ, et al. Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Ann Emerg Med. 2008;52:(6)714-48. [pubmed]

4.Hwang V, Trickey AW, Lormel C, et al. Are pediatric concussion patients compliant with discharge instructions? J Trauma Acute Care Surg. 2014;77(1):117–22; discussion 122.

5. Brown NJ, Mannix RC, O’Brien MJ, Gostine D, Collins MW, Meehan WP. Effect of cognitive activity level on duration of post-concussion symptoms. Pediatrics. 2014;133(2):e299–304.

6.Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135:(2)213-23. [pubmed]

Answers

 1.  D.  The patient presents with minor head trauma and complaints consistent with a concussion and should have neurology follow up arranged. A concussion is a minor TBI that is often seen in MVCs and collision sports (football, hockey). It is typically caused by a rotational injury or an acceleration-deceleration injury. Patients will present with a number of non-specific symptoms including headaches, dizziness, confusion, amnesia, difficulty concentrating, and blurry vision but do not have focal neurologic findings. Despite the absence of severe intracranial injury, patients can have chronic and debilitating symptoms from concussions. Neurology referral is recommended, as patients should have functional testing and tracking of their symptoms for resolution. It is vital to counsel patients to avoid contact sports or activities that increased the risk of recurrent injury as these patients are at risk for more severe injury with second impact.In the absence of focal neurologic findings, absence of antiplatelet or anticoagulant use and minor trauma, imaging is not needed (A, B, C).

2. Cerebral concussions are clinically characterized by headaches, confusion, dizziness, and amnesia for the event. Concussions are characterized by a transient loss of consciousness that occurs immediately following blunt, nonprenetrating head trauma, caused by impairment of the reticular activating system. Concussions present without focal neurologic deficits, and CT and MRI show no acute abnormalities. Although not commonly performed for concussions, functional imaging, such a PET scan, may show changes in blood flow and glucose uptake. It is critical to inform the patient and his or her family of the second impact syndrome (SIS), which occurs when a patient suffers a second concussion after being symptom-free from the first. Although SIS is more common in sports based injuries, especially among teenagers, the risk of serious sequelae following a second concussion is immense. Due to neurochemical and autoregulatory changes that may still be present, a second concussion soon after a first generally produces a rapid neurologic decline that proves fatal. Patients should be told to avoid activities that could cause falls or trauma for at least 1 week after the patient is completely asymptomatic from the first concussion. Most patients with a concussion can be discharged from the emergency department and advised to follow-up with a primary care physician within 1 week (B). Although some patients have only transient symptoms from a concussion, others may experience persistent symptoms termed postconcussive syndrome (PCS).  PCS symptoms most often include headache as well as memory, sensory, sleep, and concentration disturbances. It is important to consider PCS in all patients with a concussion, but a primary care physician is generally able to care for these patients. It is unnecessary to obtain an MRI (C).  Although patients should avoid trauma and falls for at least 1 week after being completely asymptomatic after the first concussion, a change insleeping position (D) is unnecessary.

PlayPlay

FOAMcastini – Reflections on ACEP tPA Clinical Policy Update Draft

(iTunes or Listen Here)

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
PlayPlay

Episode 22 – The Knee

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

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. [polldaddy poll=8568492]

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. [polldaddy poll=8569540]

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.

PlayPlay

Episode 21 – Acute Kidney Injury

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

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%. [polldaddy poll=8545511]

Question 2.  A 54-year-old man presents to the ED in acute renal failure (ARF). [polldaddy poll=8545512]

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 19 – Environment: Mushrooms and Hypothermia

(ITUNES OR LISTEN HERE)

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.

Screen Shot 2014-11-22 at 9.30.13 PM

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.[polldaddy poll=8469565]

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

Question 3.

[polldaddy poll=8473489]

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.

PlayPlay

Episode 18 – Falls and Geriatrics

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

We review Dr. Ken Milne’s podcast, The Skeptic’s Guide to Emergency Medicine Episode #89,  special episode on falls in the geriatric.  This episode is the first in the HOP (Hot Off the Press) series in which Dr. Milne has paired with Academic Emergency Medicine and the Canadian Journal of Emergency Medicine to review a paper, with the author, the same week the paper is published.

Why HOP is special:

  • Reducing the knowledge gap by disseminating hot-off- the press
  • Concurrent peer review from global audience.  Peer review is a flawed process and in this way, Dr. Milne takes his skeptical perspective to the paper and the author.
  • Key comments from social media will then be published in these journals, reaching the traditional academic readership.

Pearls from the Carpenter et al systematic review

Fall Statistics:

  • Fall Rates – > 65 y/o – 1 in 3 people fall per year; > 80 years old – 1 in 2 people fall per year
  • Elderly patients who fall and are admitted have a 1 year mortality of ~33% [1,3]. So, geriatric falls are bad, it seems logical to wish to predict who is going to fall.

Predictors of Falls:

  • The best negative likelihood ratio (-LR) was if the patient could cut their own toenails –LR 0.57 (95% CI 0.38-0.86) (remember, the target for a -LR is 0.1). This outperformed traditional assessments like the “get up and go test.”
  • Previous history of falls is a big predictor of falls.  Of elderly patients who present to the ED with a fall, the incidence of another fall by 6 months later is 31%.  Of those patients who present with a fall as a secondary problem,14% had another fall within 6 months.
  • The Carpenter instrument has a promising -LR of 0.11 (95% CI = 0.06-0.20) but has not been validated
    • Carpenter instrument: Nonhealing foot sores, self-reported depression, not clipping one’s own toenails, and previous falls

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (6e) Chapter 307 (This chapter was removed from the seventh edition) ; Rosen’s 8(e) Chapter 182 – but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Abdominal Pain Abdominal pain in the elderly is much higher risk than the younger cohort. This is complicated by vague presentations.  Abdominal pain in the elderly often causes one to raise an eyebrow and ponder chest pathology such as an atypical presentation of ACS.  However, the converse can also be true.  Chest discomfort may really reflect intra-abdominal pathology.  Bottom line – presentations are vague and badness is common.

Geriatric abdominal pain stats:

  • Fever and WBC unreliable.  Per Rosen’s “Elders with potentially catastrophic intra-abdominal processes may not present with a fever or an elevated white blood cell count.”
  • Much higher risk than younger patients – 2/3 patients admitted and 1/5 go directly to the operating room.
  • Most common serious pathologies:  Biliary pathology (cholecystitis), small bowel obstruction, appendicitis.
  • Vascular pathologies such as abdominal aortic aneurysm (AAA) and mesenteric ischemia also have an important place in the differential given increased incidence in the elderly.

FOAM resources:

Polypharmacy  Elderly patients are often on a host of medications but have physiologic alterations that make them susceptible to increased adverse events.

  • 12-30% of admitted elderly patients have adverse drug reactions or interactions as a primary or major contributing factor to their admission and 25% of these drug reactions or interactions are serious or life-threaten
  • Garfinkel et al demonstrated that reducing medications in elderly nursing home patients may actually be better for their health.
  • Some of the highest risk medications, in general, for our elderly patients: diuretics, nonopioid analgesics, hypoglycemics, and anticoagulants.  A patient’s presentation (syncope, fall) may be a manifestation of a medication side effect.
  • There are many high risk pharmaceuticals in the ED, but be very cautious of: narcotics, nonsteroidal anti-inflammatory agents, sedative-hypnotics, muscle relaxants, and antihistamines.
    • NSAIDS – patients may have reduced renal function and due to loss of lean muscle mass, creatine may not be accurate and NSAIDs may tip the patient into renal insufficiency. These drugs may also worsen hypertension and congestive heart failure as a result of salt retention.  NSAIDs are also associated with gastrointestinal bleeding.  Be cautious – acetaminophen is the safer bet.
    • Narcotics – may predispose patients to falls (which are bad in the elderly).  These drugs may also constipate patients, which can cause abdominal pain.  Give guidance and make sure the patient has a solid bowel regimen.
  • Start low and go slow.  It’s much easier to add doses of medications than clearing excess medications.
  • Cautiously start new medications. Furthermore, as drugs may be responsible for the patient’s symptoms that brought them to the ED, review the medication list. If possible, consider discussing discontinuation of medications with the patient’s PCP.

FOAM resources:

Delirium – Delirium in the elderly ED patients is associated with a 12-month mortality rate of 10% to 26% [5].  Be wary of chalking up alterations in mental status to dementia or sundowning.

 

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1. [polldaddy poll=8443367]

Question 1. An 87-year-old woman presents to the ED after her caregiver witnessed the patient having difficulty swallowing over the past 2 days. The patient is having difficulty with both solids and liquids. She requires multiple swallowing attempts and occasionally has a mild choking episode. She has no other complaints. Your exam is unremarkable. [polldaddy poll=8443380]

Bonus Question: What proportion of elderly patients with proven bacterial infections lack a fever?

References:

1.Carpenter CR, Avidan MS, Wildes T, et al. Predicting Geriatric Falls Following an Episode of Emergency Department Care: A Systematic Review. Acad Emerg Med. 2014 Oct;21(10):1069-1082.

2. “The Elder Patient.” Chapter 182.  Rosen’s Emergency Medicine, 8e.

3.  “The Elderly Patient.” Chapter 307.  Tintinalli’s Emergency Medicine: A Comprehensive Review, 6e.

4. Garfinkel D1, Zur-Gil S, Ben-Israel J. The war against polypharmacy: a new cost-effective geriatric-palliative approach for improving drug therapy in disabled elderly people.  Isr Med Assoc J. 2007 Jun;9(6):430-4.

5. Gower LE, Gatewood MO, Kang CS. Emergency Department Management of Delirium in the Elderly. West J Emerg Med. May 2012; 13(2): 194–201.

Answers:

1.D.  Physiologic changes of aging affect virtually every organ system and have many effects on the health and functional status of the elderly. Compared to healthy adults, elderly patients have a decreased thirst response that puts them atincreased risk for dehydration and electrolyte abnormalities. Cell-mediated immunity (A) is decreased, which increases susceptibility to neoplasms and a tendency to reactivate latent diseases. Peripheral vascular resistance (B) is increased contributing to development of hypertension. Sweat glands (C) are decreased in the elderly, which puts them at risk for hyperthermia.

2.B.  Dysphagia can be divided into two categories: transfer and transport. Transfer dysphagia occurs early in swallowing and is often described by the patient as difficulty with initiation of swallowing. Transport dysphagia occurs due to impaired movement of the bolus down the esophagus and through the lower sphincter. This patient is experiencing a transfer dysphagia. This condition is most commonly due to neuromuscular disorders that result in misdirection of the food bolus and requires repeated swallowing attempts. A cerebrovascular accident (stroke) that causes muscleweakness of the oropharyngeal muscles is frequently the underlying cause.
Achalasia (A) is the most common motility disorder producing dysphagia. It is typically seen in patients between 20 and 40 years of age and is associated with esophageal spasm, chest pain, and odynophagia. Esophageal neoplasm (C)usually leads to dysphagia over a period of months and progresses from symptoms with solids to liquids. It is also associated with weight loss and bleeding. Foreign bodies (D) such as a food bolus can lead to dysphagia, but patients are typically unable to tolerate secretions and are often observed drooling. These patients do not have difficulty in initiating swallowing.

Bonus. Up to one half.

PlayPlay

FOAMcastini – SMACC

(ITUNES OR LISTEN HERE)

FOAMcast will be back shortly with regular core content-cutting edge mash ups.  However, we would be remiss not to take a moment to focus on a conference that inadvertently created FOAMcast…and is coming to Chicago in June 2015.  SMACC – Chicago (#smaccUS) June 23-26, 2015.

The etiology:  FOAMcast was dreamed up whilst milling around the exhibition hall at SMACC, discussing how even core content and “basic” medicine seemed cutting edge and important here.  These projects can be dreamed up via Twitter or e-mail but I think there’s something special engendered by the propinquity of Free Open Access Medical education (FOAM) mixed with the physical conference. Our fate was sealed when Dr. Victoria Brazil happened to stop by to say “hi” while we were hyped up on “long blacks” and blabbering away about what we would call our project.  For better or worse, FOAMcast was born.

  • Note: Please do not blame Dr. Brazil for our off-beat humor or the podcast.  She had no idea what we were up to and does not endorse FOAMcast or Drs. Jeremy Faust and Lauren Westafer.

The talks at SMACC were unparalleled.  The speakers inspiring, the slides clean, the material relevant, and the audience questions thoughtful.  We learned from social workers (Liz Crowe’s hilarious talk), nurses, medics, and doctors from around the globe.  In fact, we became friends, even the pre-med university student.  We learned from them all.

The Core Content – There were a cornucopia of excellent core content talks; for example, Natalie May’s pediatric pearls, Aortic Catastrophes, and the Meaning of Acidosis by Dr. David Story.  There are too many to list and they’re all worth a listen and can be found on iTunes or via the Intensive Care Network.  Even the sonowars were brilliant.  For example, Drs. Matt Dawson and Mike Mallin taught us to visualize cardiac view using humans.  The awkward apical 4 chamber view for cardiac ultrasound:

Apical 4 Chamber View - Cardiac Ultrasound
Awkward (Apical) 4 Chamber View – Cardiac Ultrasound

In this episode, we only had time to hit just a few heavy hitters that haven’t made it onto our other podcasts.

Dr. Haney Mallemat – The Art and Science of Fluid Responsiveness

  • Dr. Mallemat beautifully describes various methods of assessing fluid responsiveness – from IVC ultrasound (used alone, approximately equal to CVP), stroke volume variation, to passive leg raise and more advance ultrasound techniques.
  • Use dynamic markers rather than static numbers, which seemed to be universally lousy.  Trend the patient’s response in order to give them “as much fluid as they need, and not one drop more.”

Dr. Scott Weingart – Sepsis in New York: Our First 15,000 Patients

  • Source control is key in sepsis.  If a patient has an infected gallbladder, obstructing kidney stone, etc – call surgery. Advocate for these patients.
  • ProCESS (and now ARISE) have demonstrated that protocols don’t necessarily have to be followed in order to reduce mortality in sepsis.  We have become increasingly good at identifying and treating sepsis since the original EGDT trial.  In his words – you don’t have to do sh*t, you just have to give a sh*t (Note: you still have to provide basic resuscitation, antibiotics, etc; you just don’t have to do the fancy stuff).
  • He had more pearls about lactate – such as in his collaborative, the number predicted badness but trends mattered less.

Dr. Cliff Reid – Resuscitation Dogmalysis

  • One cannot predict blood pressure based on the presence or absence of a pulse in various anatomic locales (i.e. if there’s a pulse at the radial artery, then their systolic blood pressure is at least >80 mmHg).  This myth was taught for years and still persists in some trauma bays; however, even the evidence and the two most recent iterations of ATLS agree with Dr. Reid [Deakin et al]

Dr. Rob Mac Sweeney – ARDS: An Evidence Based Update

  • The Berlin definition of ARDS [ARDS Definition Task Force]:
    • Acute worsening of respiratory failure (< 1 week)
    • Edema not solely due to hydrostatic pulmonary edema (i.e. should not be due to heart failure or fluid overload)
    • Bilateral infiltrates on CT/CXR *(subjective)
    • PaO2/FiO2 ratio <300 mmHg with at least 5 cm H20 of PEEP
  • The premise of Dr. Mac Sweeney’s talk; however, is that we ARDS is problematic because:
    • ARDS is a disease we can’t diagnose –  Many of the criteria, although seemingly helped by the Berlin definition, are still subjective (ex: CXR Sensitivity 0.73; specificity, 0.70 [Figueroa-Casas]
    • The diagnosis of ARDS is of limited clinical utility.  What he means by this is that the definition doesn’t really affect management and nearly all drugs targeted towards ARDS fail to show benefit consistently.  The ARDS care that does work, like lung protective ventilation and fluid balance, these are just good critical care.  Proning may work, but doesn’t seem to pan out in everyone [Guerin].  Dr. Mac Sweeney is also a little sweet on ECMO, awaiting future studies.
    • People don’t typically die from ARDS even though ARDS is associated with a 40-50% mortality rate.  Yet, only 10% of people with ARDS die of ARDS or respiratory failure. Most people with ARDS die because they’re super sick.
    • Most people with ARDS don’t have ARDS.  Autopsy studies have demonstrated that ~50% of people who met Berlin criteria for ARDS didn’t have the pathognomonic feature of ARDS, diffuse alveolar damage (DAD). The other half of the patients had pneumonia, abscesses, COPD, or other processes [Pinheiro et alThielle et al].
  • The crux of the ARDS issue per Dr. Mac Sweeney -It seems that ARDS is a fairly diverse spectrum with some subjectivity to the criteria.  If approximately half of the people diagnosed with ARDS don’t have ARDS, then it’s no surprise that the therapies don’t benefit them.  He leaves better identification in the hands of researchers.

Timing, Tribes, and STEMIs

  • In medicine we use teams or “tribes” to cope with stress, work together, and rally – Tribe Emergency Medicine, Tribe Anesthesiology, Tribe Surgery, etc.  While making snarky comments, if in jest, may boost the morale and confidence of our team, this may be detrimental to overall patient care
SMACC GOLD
SMACC – Built Friendships, Adventures, and Better Learners
PlayPlay

FOAMcastini – ACEP Round Up #2

(ITUNES OR LISTEN HERE)

FOAMcast is bringing you pearls from conferences we attend and, first up, the American College of Emergency Physicians annual meeting, ACEP14.  Yesterday’s episode covered the council meetings.

Scientific Assembly Day 1 Pearls

Opening Session by Freakonomics hosts Steven Levitt and Stephen Dubner. Weird choice? It turns out that economists and physicians have a lot in common.  What’s that?  Probabilities.  As physicians we like to think of ourselves as diagnosticians, but we’re more like probalisticians.  We make predictions, hopefully based on the best evidence, our clinical expertise, and our patient’s values.  People don’t remember the little stuff, like extra testing but they do tend to remember the more outlandish things, like the “amazing saves” or awful “misses.”

  • See this post by Dr. Simon Carley, in which he describes the ways in which physicians are really playing the odds and gambling.

Cardiology Pearls from Dr. Slovis.

  • Post cardiac arrest – targeted temperature management to 35-36 Celsius is the new 33 Celsius [Nielsen].
  • Many patients should probably go to the cath lab after arrest, but it’s still not clear exactly who benefits the most.  STEMIs should probably go to the cath lab and, perhaps, non-STEMI ventricular fibrillation/tachycardia arrests.  Apparently, 10-30% of these are actually STEMIs “on the inside” [More skeptical takes on this from Dr. Radecki here and here]

Infectious Disease Pearls from Dr. David Pigott – When someone returns from a developing nation, say, West Africa, the cause of their fever is not necessarily ebola. It’s probably an unknown, regular virus.   It’s probably not ebola but it may be malaria which is quite common.

  • His thoughts on predictors of badness: Symptoms typically appear within 8-10 days although the “watch” period is 21 days.  If a patient is in their second week of symptoms and are hemodynamically stable, then the patient has a pretty good shot.

Tox Pearls from Dr. Tim Erickson

  • Calcium channel blocker toxicity – you can try fluids, calcium, atropine, and vasopressors.  For sick patients, however, insulin is the best bet (Note, FOAM is ahead of the curve: post on the lack of utility in glucagon from 2012).
    • Insulin bolus of 1 unit/kg followed by a drip of 1 unit/kg/h.  Add dextrose at about 0.5 mg/kg/h, depending on their glucose.
    • Check glucose and potassium every 30 minutes, with the goal to keep the potassium 2.8-3.2, per Goldfrank.
  • Cyanide toxicity (discussed here) – if you’re thinking about it, please do NOT wait on a cyanide level, or any labs.  Treat, with the current recommendation of intravenous hydroxocobalamin. There’s some discussion on the use of intramuscular cobinamide, which would be great in situations without IVs; however, this is largely untested in humans presently [Bebarta et al].
  • Beware of cognitive biases, such as anchoring. For example, lactic acidosis isn’t always sepsis, cyanide, or carbon monoxide.  Metformin associated lactic acidosis is also a thing.

Dr. Scott Weingart – Catch the CO2 Wave (podcast).  End tidal CO2 (ETCO2) – ETCO2 has become essential in monitoring patients in the ED.  With anything we monitor, we really need to understand what we’re looking at as well as the interventions.

  • ETCO2 does NOT = PaCO2.
  • In most patients, the PaCO2 will be ~3-5 mmHg higher than their ETCO2.
  • This is because ETCO2 is really a measure of: PaCO2 (or production) but also cardiac output and alveolar ventilation.  Thus, the ETCO2 may be falsely low in a patient with significant dead space, such as COPD, or with impaired cardiac output (heart failure).

For updates, follow #ACEP14

10660263_10102341624362828_5347687688294499115_n

Episode 16 – Headaches

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

This week we review a post from Dr. Rob Orman’s ERCast, Is it really a sinus headache?

POUND- 4 criteria is very indicative of migraine (+LR 24), 3 criteria also likely (+LR 3), although most of this comes from the outpatient literature [1].

  • Pounding headache
  • hOurs: headache lasts 4-72 h without medication
  • Unilateral headaches
  • Nausea
  • Disabling: disrupts daily activities

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 159 ; Rosen’s 8(e) Chapter 20, 103 – but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

In Emergency Medicine, our job is to investigate and think about the life and limb threatening causes, even to mundane problems.   Things such as intracranial bleeds, meningitis, masses – these are huge deals and are covered well and hammered into our heads.  For FOAM core content on this, check out the St. Emlyn’s podcast.  On this episode, we’re running a mini-ophthalmology headache special and focusing on headaches that treatment may render “sight saving.”

Temporal Arteritis – often in patients older than 50 years of age and more common in those with a history of polymyalgia rheumatica. May be accompanied by visual changes including the “classic” amaurosis fugax or “curtain” of unilateral vision loss.  If not treated, these patient can lose vision permanently.

  • Unilateral or localized headache, often in the temporal or retro-orbital area
  • Jaw claudication (pain with chewing) – most specific sign
  • Decreased pulse in temporal artery or tenderness
  • Sedimentation Rate (ESR) >50

Treatment

  • Prednisone 40-60 mg if thinking about diagnosis
  • Temporal artery biopsy within 48 hrs

Acute Angle Closure Glaucoma – Classically, these patients present with unilateral mid-dilated pupils and severe nausea, vomiting, and headaches.  The history can, naturally, be less classic and more vague.  Also, if not treated, this can lead to vision loss.

  • Elevated intraocular pressure (>20 mmHg)
  • Decreased visual acuity
  • Fixed irregular semidilated (midposition) pupil
  • Slit lamp — shallow AC (closed angle), injected conjunctiva; corneal microcystic edema (cloudy)

Treatment –

  • Ophthalmology consult stat
    • They may want topical b-blocker, cholinergic, alpha-2 agonist, eye drops or administration of acetazolamide

Idiopathic Intracranial Hypertension (Pseudotumor Cerebri) – Common in young, overweight women or those on oral contraceptives.  Untreated, they can suffer vision loss.

  • Elevated opening pressure (>20-25 cm H20) on lumbar puncture

Treatment

  • Neuro follow up
  • Acetazolamide +/- furosemide
  • Therapeutic lumbar punctures

Cerebral Venous Sinus Thrombosis – may present as atypical headache with stroke like symptoms in patients without known vascular risk factors.  The neurological findings may be transient.  Often associated with post-partum patients, patients with hypercoaguable states (Factor V mutations, protein C or S deficiency, antithrombin III deficiency, etc), patients on OCPs.

Diagnosis – CTV or MRV (magnetic resonance venography) after CT scan, which may be normal.

Treatment – Anticoagulation, although this is somewhat controversial

Generously Donated Rosh Review Questions (Scroll for Answers)
Question 1. A 73-year-old woman with a history of hypertension presents with a unilateral headache for 3 weeks. She states that she has a throbbing pain at her right temple and has pain in her jaw with opening and closing. The vision in her right eye has worsened over the previous day. Her blood pressure is 173/100.
 [polldaddy poll=8340282]
Question 2. A 71-year-old woman presents to the ED with daily headaches for 2 months. She describes the headache as a dull pain that is most intense in the morning and resolves by the afternoon. On exam you note 4/5 motor weakness of the left upper and lower extremity.
[polldaddy poll=8340292]
References:
1. Detsky ME,McDonald DR, Baerlocher MO, Tomlinson GA,McCrory DC, Booth CM. Does this patient with headache have a migraine or need neuroimaging? JAMA. 2006 Sep 13;296(10):1274-83.

2. Chapter 20, 103.  Rosen’s Emergency Medicine, 8e.

3.Chapter 159.  Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011

Answers
1. D. This patient presents with a unilateral, subacute headache with associated jaw claudication and vision change; symptoms consistent with temporal arteritis. Temporal arteritis or giant cell arteritis is a systemic inflammatory process of small and medium-size arteries. The most commonly involved vessels are the ophthalmic vessels and the extracranial branches of the aortic arch. The disease typically affects patients over 70 years of age and is more common in women than in men. Patients present with a subacute headache that is throbbing in nature and may be present for weeks to months. Often, patients will have symptoms for more than 2 months. Patients may also report jaw claudication secondary to vascular insufficiency of the masseter and temporalis muscles. Physical examination may reveal tenderness over the temporal artery. Systemic symptoms may also be present including fever, joint pains, and weight loss. Diagnostic testing in the Emergency Department generally begins with an erythrocyte sedimentation rate (ESR) with a cutoff of 50 mm/hour although the level may be >100 mm/hour. However, the ESR will be normal in 10-25% of patients. The gold standard diagnostic test is a temporal artery biopsy. In patients with a high-clinical likelihood of temporal arteritis, treatment should be initiated regardless of initial diagnostic testing as delay can lead to permanent visual loss. Prednisone should be started at 60 – 120 mg/day.

Carbamazepine (A) is the treatment of choice for trigeminal neuralgia, not temporal arteritis. The patient does not present with symptoms consistent with hypertensive emergency requiring emergent antihypertensive treatment withlabetalol (B). A non-contrast head CT scan (C) is not helpful in temporal arteritis as the disease does not involve the intracranial contents.

2.  B  More than half of patients diagnosed with a brain tumor complain of headache. However, the headache associated with brain tumor is highly variable. Patients may describe it as continuous or intermittent, unilateral or bilateral, sharp or dull. It is associated with neurologic deficits less than 10% of the time. However, in the setting of aneurologic deficit and chronic headache (as in this scenario with motor weakness), a mass lesion should be strongly considered as the cause. Patients may also complain of nausea, vomiting, visual change, and gait disturbance. Headaches due to brain tumors are classically associated with pain that is worse in the morning (as in this case). However, this is rare.

Central venous thrombosis (A) results from hypercoagulable states and is associated with acute to subacute headaches with vomiting and sometimes seizures. Risk factors include the use of oral contraceptives, postpartum or postoperative states, and any hypercoagulable state such as factor V Leiden mutation, antithrombin III deficiency, protein S or C deficiency, or polycythemia. The diagnosis is usually made by MRI venogram. Migraine headache (C) is classified as a primary headache and can be quite variable in presentation. These headaches can be associated with nausea, vomiting, photophobia, and phonophobia. The headache may also be preceded or accompanied by an aura that develops gradually over minutes, usually lasts 60 minutes, and is reversible. Auras may include neurologic symptom but commonly include scintillating scotomas (dark spots) or flashing lights. Temporal arteritis (D) occurs almost exclusively in patients older than 50 years and is much more common in women. Headache is the most common symptom of temporal arteritis and usually occurs over the frontotemporal region. It is strongly associated with a history of polymyalgia rheumatic. It is not associated with focal neurologic deficits, but it can lead to vision loss due to ischemic optic neuritis.