The Role of the CVP in a Post- “7 Mares” Era
 

The role for using central venous pressure (CVP) as a measure of volume responsiveness has largely fallen out of favor over the years.¹ There are certainly better indices for fluid responsiveness, but don’t be fooled – the CVP isn’t a one trick pony.  In fact, a high or rapidly rising CVP should raise a significant concern for impending cardiovascular collapse.

Consider the following differential diagnosis in the patient with an abnormally high or rising CVP ( >10 cm H₂O).

• Excessive pressures outside of the heart or impediments to venous return (juxta-cardiac pressures)
  • Cardiac tamponade
  • Auto PEEP or breath stacking during mechanical ventilation
  • Tension pneumothorax
• Venous return that’s more than the right ventricle can handle
  • RV failure
  • Severe tricuspid valve disease
  • Massive increase in pulmonary vascular resistance (massive PE, pulmonary hypertension, ARDS, LV failure)

Bottom Line: In a time where the utility of the CVP has been largely dismissed, remember that an abnormal CVP offers great deal of information beyond a simple measure of volume status.

References

1. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134(1):172-8.
2. Berlin DA, Bakker J. Starling curves and central venous pressure. Critical Care. 2015;19(1):55.

Follow me on Twitter: @JohnGreenwoodMD

Question

45 year-old male complains of pleuritic chest pain following a "long" flight. What's the diagnosis and what's this sign called?

Show Answer

Show References

This study is a case control study of the association of congenital heart disease (CHD) and stroke using a base population of 2.5 million Kaiser patients in California. 412 cases of stroke were identified and compared to 1236 controls. Of these stroke patients, 11/216 ischemic strokes and 4/196 hemorrhagic strokes were attributed to CHD (both cyanotic and acyanotic lesions). CHD was found in 7/1236 controls.

Children with CHD and history of cardiac surgery had the strongest risk of stroke (31 fold over the control group). Many of these children had strokes years after their surgery. Children with CHD who did not have cardiac surgery had a trend towards elevated stroke risk, but the confidence intervals included the null. More children without CHD history presented with headache.

Bottom line: Stroke risk (both hemorrhagic and ischemic) extend past the immediate postoperative period in patients with CHD.

Show References

The Centers for Disease Control continues to report increased numbers of measles patients in the US. From January 1 to February 13, 2015 there have been 141 cases.  It has spread to 17 states and the District of Columbia, with 80% linked to the multistate outbreak from Disneyland.

Measles is not a benign disease!

Per the World Health Organization, there were 146,700 measles deaths globally in 2013.  Most of these deaths occur in lower- and middle-income countries,

Even in the US, measles can cause serious complications and death. Complications from measles can be seen in any age group, but particularly in children <5 years of age and in adults >20 years of age.

Measles Complications:

Common:

• Ear infections (about 1 in 10 children)
  • Can result in permanent hearing loss
• Diarrhea (about 1 in 10 people with measles)

Severe:

• Pneumonia (as many as 1 in 20 children)
  • Most common cause of death
• Encephalitis (about 1 in 1,000 children)
  • Can lead to seizures, hearing loss, intellectual disability
• Death (1 to 2 per 1,000 children)
• Measles in pregnancy can cause premature birth and low-birth-weight babies

Long-term:

• Subacute sclerosing panencephalitis (SSPE)
  • Aside from the long-term complications above, an estimate 4 to 11 out of every 100,000 will develop this fatal disease of the central nervous system 7 to 10 years after infection.

Bottom Line:

Per Dr. Anne Schuchat of the CDC: “This is not a problem with the measles vaccine not working. This is a problem of the measles vaccine not being used.”

Show References

Show References

Question

Show Answer

Show References

The Unforgotten: ECG Utilization to Differentiate Athletic Heart vs. Brugada

- Highly trained athletes develop ECG changes as a physiologic consequence of increased vagal tone; The ECG manifestations of early repolarization (ER) can range from simple J–point elevation to anterior (V1 to V3) "domed" ST-segment elevation and negative T wave.

- The former raises problems of differential some forms of ER with the “ coved-type” pattern seen in Brugada Syndrome (BS).

- A recent study compared the ECG tracings of 61 athletes w/a “domed” ST-segment elevation & negative T wave and 92  age/sex-matched BS patients w/a “ coved-type” pattern to identify an ECG criteria for distinguishing benign athletic changes seen in ER from BS.

- ECG analysis focused on ST-segment elevation at J-point (STJ ) and at 80 milliseconds after J-point (ST80 ).

- Athletes had a lower maximum amplitude of STJ  (p < 0.001) & lower STJ /ST80 (p < 0.001)

- All patients (100%) with BS showed a downsloping ST-segment configuration (STJ/ST80 > 1) versus only 2 (3%) athletes (p < 0.001)

- An upsloping ST-segment configuration (STJ /ST80 < 1) showed a sensitivity of 97%, a specificity of 100%, and a diagnostic accuracy of 98.7% for the diagnosis of ER.

A: ER

B: Brugada 

Show References

LATERAL ANKLE TENDINOPATHY

Hx: subacute onset (weeks) of the pain seen in athletes esp. runners (banked or uneven surfaces).

PE: Tenderness to palpation posterior to the lateral malleolus or over the course of the tendon. Pain worse with resisted ankle eversion from a dorsiflexed postion. Examine for subluxation of tendon.

The diagnosis is made from the above and does not require imaging.

Tx: Rest, conservative care, physical therapy (eccentric exercise focus), ankle taping or lace up brace. Severe cases may even require a walking boot.

http://www.epainassist.com/images/Article-Images/Peroneal_Tendonitis.jpg

Pediatric Caffeine Overdose

As the in-service draws closer and the hours to study wind down, I find myself becoming more and more of a caffeine enthusiast. While a No-Doz or Diet Mt. Dew may put a little more pep in my step, the caffeine found in energy drinks, caffeine pills, and diet supplements can quickly result in an dangerous overdose in a young child.

Caffeine Overdose Presentation- Sympathomimetic Toxidrome

• Tachycardia, dysrhythmia, hypertension
• Diaphoresis, piloerection
• Nausea, vomiting
• Hyperthermia
• Dilated pupils
• Agitation, delusions, paranoia
• Seizures, coma
• Sometimes: Metabolic acidosis, hypokalemia
• Rhabdo- muscle breakdown by Ca++ sequestration in the sarcoplasmic reticulum

Available Sources of Caffeine-

• NoDoz- 200mg/tab
• Excedrin 65mg/tab
• Starbuck Double Shot 130mg/6.5oz
• Monster Energy Drink 160mg/16oz
• Caffeine Solution for Neonates with Apnea of Prematurity
• So many more!

Toxic Doses

• 15 mg/L- tachycardia, arrhythmia, HTN, seizure, vomiting, irritable, delusions, hallucinations (approx 1500 mg for an adult)
• >80 mg/L- Coma or Death

Management- treat the symptoms (metabolic, cardiovascular, and neurologic)

• IV Fluids
• Anti-emetics
• Sodium Bicarb if refractory metabolic acidosis
• Benzos for severe agitation or seizure
• PALS protocols for cardiac arrhythmias

Good Luck on the In-Service!

Show References

A new review summarized published adverse effects when IV lipid emulsion is used along with venous-arterial extracorporeal membrane oxygenation (VA-ECMO) in patients with cardiotoxic drug poisoning.

Not surprisingly, running fat through the ECMO circuit can cause some issues. Here's what's been published:

• cracking of stopcocks
• fat emulsion agglutination
• clogging and associated malfunction of the membrane oxygenator
• increased blood clot formation in the circuit

It's unclear how these findings should change management if using both treatment modalities, but at the very least, be aware that fat depostion in the VA-ECMO circuits and increased blood clot formation can occur.

Show References

Magnesium, another failed neuroprotectant?

Stroke is a leading cause of adult disability and the second leading cause of death worldwide.  Currently available therapies for acute ischemic stroke are based on restoring perfusion to the ischemic penumbra. However, they are only moderately effective.

A series of pathological cascades leading to neuronal death are triggered in acute ischemia.  Thus it may be logical to suggest that if one can interrupt the propagation of these cascades, perhaps part of the brain tissue can be protected and salvaged.

Magnesium has been shown in various animal models to have pluripotent neuroprotective properties.  It is also widely available, simple to administer, and has a favorable risk profile.  A prior study of magnesium in acute ischemic stroke (IMAGES) did not show a benefit when the agent was administered a median 7.4 hours after symptom onset.  However, a subgroup of patients treated within 3 hours of symptom onset showed possible benefit.

The Field Administration of Stroke Therapy - Magnesium (FAST-MAG) trial, funded by the NIH, looked at magnesium administered within 2 hours after symptom onset on the degree of disability at 90 days after stroke as measured by the modified Rankin scale.

• A total of 1700 patients were included in the study.
• 73.3% of patients had a final diagnosis of ischemic stroke, compared with 22.8% with intracranial hemorrhage and 3.9% with stroke-mimicking condition.
• Of the patients with ischemic stroke, 52.4% were treated with tPA.

Magnesium was not found to have any benefit in functional outcome at 90 days.

This study was unique in several ways:

• It examined the use of a neuroprotective agent in the hyperacute window of 2 hours, as a common criticism of prior neuroprotective studies is that those agents may not have been administered within the optimal therapeutic window
• Administration of the neuroprotective agent began in the prehospital setting.  Logistically, this was done with a pre-randomized study kit containing the initial bolus dose to be administered by EMS and the maintenance dose to be given to the receiving hospital for administration in the ED.
• Despite the short window for enrollment and drug administration, patients were screened using a previously validated prehospital stroke scale and 98.7% of patients were enrolled after explicit written informed consent from the patient or a legally authorized representative.

However, despite this study being very well executed, demonstrating the feasibility of conducting a phase 3 trial with targeted intervention within the hyperacute window, it is another neuroprotective agent that failed to translate from the laboratory bench to the clinical realm.

Potential explanations for the discrepancies between preclinical and clinical outcomes of neuroprotective agents thus far include discrepancies on outcome measures, functional assessments, pre-morbid conditions, therapeutic windows, and drug-dosing schedules between animal studies and clinical trials.

Take Home Point: Magnesium does not have any clear benefit in acute ischemic stroke at this time.

Show References

Updates in preventative strategies in the ICU

Preventing Ventilator Associated Pneumonia (VAP)

• Traditionally ICUs use techniques such as head of bed elevation> 30 degrees, chlorhexidine mouth rinses, reduced sedation, and controlling cuff pressure between 20-30 cm H2O to reduce VAP
• A new trial confirms that subglottic suctioning also reduces VAP
• Endotracheal tubes are made with a suction line along the edge with fenestrations below the vocal cords and above the cuff
• This is hooked to wall suction removing secretions before they are aspirated
• VAP rates are very low in the US (most likely due to under-reporting)
• It is reported at around 15 VAPs/ 1000 ventilator days in Europe

The trial

• 5 ICUs in Belgium; 352 total patients with suctioning vs control were randomized
• Reduced incidence of confirmed VAP 9% vs 18%, decrease ventilator days 10 vs 20 and antibiotic use 7% absolute reduction

Bottom Line

• More expensive around $20 or more vs $1 for a regular ETT
• NNT around 11 to prevent one VAP: it is cost efficient
• Use them in patients who will remain intubated for > 48hrs (not elective surgical patients)

Daily bathing with chlorhexidine does not reduce health care associated infections

• It is believed that daily bathing with chlorhexidine antibiotic washes decrease rates of infection in the ICU; this is debatable

The trial

• One center, 5 ICUs, 9340 patients
• 10 week cleaning period followed by a two week washout then crossover to the alternate treatment (non-antibiotic washes)
• Looking for CLABSIs, CAUTIs, VAP and C. diff infections
• 55 infections occurred in the chlorhexidine group; 60 in the control goup.
• 2.86 per 1000 patient days (chlorhexidine group) vs 2.9 per 1000 patient days (control)

Bottom Line

• Does not appear to be helpful (perhaps specific patient groups such as bone marrow units may benefit)
• More expensive to use these washes and can lead to resistance
• Very well designed study with a variety of ICUs used (although one center)

Show References

We know vancomycin should be dosed based on weight rather than the default 1 gm dose so many patients receive. A past Academic Life in EM post explores the nuances of proper vancomycin dosing. But do higher loading doses in the ED actually lead to more therapeutic trough levels?

New Data

A new randomized trial compared ED patients receiving 30 mg/kg initial doses vs. 15 mg/kg. [1] There was a significantly greater proportion of patients reaching target trough levels of 15 mg/L at 12 hours among the patients who received a 30 mg/kg loading dose as compared with a traditional 15 mg/kg dose (34% vs 3%, P < 0.01). This study did not use a max dose of 2 gm. They included patients up to 120 kg who received 3.6 gm loading doses! Patients with creatinine clearance < 50 mL/min were excluded. There was no difference in incidence of nephrotoxicity between the groups.

Application to Clinical Practice

• Advocate for change in your ED's order sets to weight-based dosing of vancomycin and remove 1 gm as a default option. [2, 3]
• While 34% attaininment of adequate trough levels still isn't great, properly loading vancomycin with up to 30 mg/kg is a step in the right direction. It also takes longer than one dose to reach steady-state levels.
• This study did not evaluate clinical cure rates, just trough levels.

Show References

(***)Values are after typical use; values in parentheses are after heavy or prolonged use.

Show References

From January 1^st to January 30^th, 2015, 102 people from 14 states were reported to have measles. This one month total is greater than the annual number of U.S. cases from 2002 to 2012.  Most of these cases are related to a large outbreak from a Californian amusement park. Measles can spread in communities without adequate vaccination (low herd immunity). The majority of the people in the US who get measles are unvaccinated. However, measles remains common in many parts of the world.

Bottom Line:

As noted in the recent ACEP Fact Sheet, “A very high index of suspicion for Rubeola is necessary especially among patients with an exposure history, travel to foreign or domestic areas where disease is present, and those without adequate immunization. Immediate isolation of these patients should be considered in the ED or other outpatient healthcare setting.”

Show References

Attachments

1502040913_Measles_Jan_2015.jpg (67 Kb)

Hypertensive Emergency Pearls

• It is well known that a hypertensive emergency is not defined by an arbitrary blood pressure reading.  Rather, it is characterized by the presence of end-organ dysfunction, often due to a sudden increase in sympathetic activation.
• When treating patients with a hypertensive emergency, consider the following:
  • Many are hypovolemic due to a pressue-induced natriuresis - give them fluids and avoid diuretics.
  • BP should be reduced in a controlled manner using short-acting titratable intravenous agents. Rapid reductions in BP can lead to organ hypoperfusion.
  • Avoid oral, sublingual, and transdermal medications until end-organ dysfunction has resolved.
  • Clevidipine is the newest agent
    • A third-generation dihydropyridine
    • Relaxes arteriolar smooth muscle
    • Rapid onset (2-4 min) and short acting (5-15 min)
    • Compares favorably with nicardipine in available studies

Show References

Question

Patient presents with right shoulder pain following minor trauma. What's the diagnosis....and what's the Cunningham technique?

Show Answer

Show References

Tetrodotoxin is lethal poison that blocks sodium channels. A famous sushi called "Fugu" is cut from a puffer fish that contains this poison. The idea is to get just enough of the toxin to cause peri-oral paresthesia but not too much to get seizures, paralysis and cardiac dysrrhythmias. A recent outbreak in Minneapolis, Minnesota was just reported in the MMWR so it can really happen anywhere, its a great read - dried puffer was bought from a market in NYC.

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6351a2.htm

2-3 mg of the toxin is lethal to an adult human. No antidote exists though I would try hypertonic sodium bicarbonate for the cardiac dysrrhythmias and appropraite supportive. If the patient survives 24 hrs, the patient will do well without sequelae if appropriately supported.

Patients with myasthenia gravis (MG) may be seen in the emergency department for symptoms that are not related to their MG, such as an upper respiratory tract infection or chest pain, for example.

The emergency physician should be careful in prescribing new medications to patients with MG, as that can precipitate a myasthenic crisis (and therefore cause significant morbidity and mortality). Below is a list of medications that are commonly implicated; an extensive list can be found on www.myasthenia.org/docs/MGFA_medicationsandmg.pdf)

• Iodinated IV contrast
• Fluoroquinolones
• Aminoglycosides
• Macrolides
• IV magnesium replacement
• Beta blockers (metoprolol and labetalol)

Show References

Extracorporeal Treatment Strategies for Acute Methanol Poisoning (When to Dialyze)

Methanol toxicity is classically included in the differential for the intoxicated patient presenting to the ED. Add a negative EtOH level, anion/osmolar gap, blindness and you have yourself a slam dunk diagnosis. The goal is to stop the liver from metabolizing methanol to formic acid. Outside of fomepizole (or old school ethanol therapy), dialysis is often discussed, but when should you actually get the nephrologist on the phone?

This month the Extracorporeal Treatments in Poisoning Workgroup released a systematic review and consensus statement to help clinicians decide when to pull the HD trigger. Their suggestions are below.

When to start HD:

1. Neurologic dysfunction: Coma, seizures, new vision deficits
2. Metabolic acidosis: blood pH ≤7.15 or persistent metabolic acidosis despite adequate supportive measures & antidotes
3. Serum anion gap higher than 24 mmol/L
4. Serum methanol concentration:
   • > 700 mg/L (21.8 mmol/L) if fomepizole therapy is given
   • > 600 mg/L or 18.7 mmol/L if ethanol treatment is given
   • > 500 mg/L or 15.6 mmol/L in the absence of an alcohol dehydrogenase blocker

Which Modality: Intermittent HD (IHD) should be used over continuous renal replacement therapies (CRRT), as you can clear the toxin faster with higher HD flows.

When to stop HD: Extracorporeal treatment can be terminated when the methanol concentration is less than 200 mg/L or 6.2 mmol/L and a clinical improvement is observed.

Bottom Line:  Consider early hemodialysis in most patients presenting with methanol toxicity.  Clinical exam and routine lab testing will likely provide enough information to determine the need for IHD, but specific methanol levels can be helpful to guide adjunctive treatment options.

Reference

Roberts DM, Yates C, Megarbane B, et al. Recommendations for the Role of Extracorporeal Treatments in the Management of Acute Methanol Poisoning: A Systematic Review and Consensus Statement. Crit Care Med. 2015;43(2):461-472.

Follow me on Twitter @JohnGreenwoodMD