The recently published BICAR-ICU study looked at the use of bicarb in critically ill patients with severe metabolic acidemia...

• Multicenter, open-label, RCT, 26 French ICUs
• Adult patients with pH < 7.2 not secondary to hypercapnia, serum bicarb < 20 not due to bicarb wasting process 
• SOFA score > 4 or lactate > 2
• No bicarb versus 4.2% sodium bicarb infusion titrated to pH >7.3
• Primary outcome: Composite measure of 28-mortality and presence of any organ failure at 7 days post-randomization
• Secondary outcomes: Need for/length of life support measures (renal-replacement, vasopressors, mechanical ventilation), SOFA score after enrollment, electrolyte effects, occurrence of ICU-acquired infections, and ICU length of stay
• Major findings:
  • No difference in primary outcome overall
  • No difference in pressor-free days, days off RRT, dialysis dependence at ICU discharge, ICU LOS
  • Bicarb group had less need for RRT during ICU stay (35 vs 52%, p=0.0009)
  • In patients with AKI and AKIN score 2-3*, the bicarbonate group had a decrease in both 28-day mortality (46 vs 63%, p=0.0166) and presence of any organ failure at day 7 (66 vs 82%, p=0.0142)
• Limitations:
  • Unblinded
  • A quarter of the control group actually received bicarb
  • No data regarding vent settings, ABGs to r/o ventilation effects on pH
  • 4.2% is not a standard concentration of bicarb used in the U.S.

Bottom Line: 

Consider administration of sodium bicarbonate for your critically ill ED patients with severe metabolic acidosis and AKI, especially if acidosis &/or renal function is not improved with usual initial measures (such as IVF, etc).

*Acute Kidney Injury Network Staging Criteria

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Froment’s Sign

Tests for motor weakness of the Ulnar nerve

Patient asked to hold piece of paper in both hands, grasping with the thumb and radial side of index finger of both hands

Examiner then pulls on the paper

Test is positive if patient flexes the thumb IP join in an attempt to hold onto paper

https://handlab.com/resources/wp-content/uploads/2014/04/June-2013-No25.jpg

Does Lactated Ringer's Raise Serum Lactate?

• Intravenous fluid administration is a cornerstone of resuscitation and the treatment of many critically ill ED patients.
• Recent publications have suggested that balanced crystalloid solutions may be better than 0.9% normal saline (NS) for select conditions.
• Lactated Ringer's (LR) is a common balanced crystalloid solution often used for fluid resuscitation in critically ill patients.
• AS LR contains approximately 28 mmol/L of sodium lactate, the question of whether LR elevates serum lacate is frequently asked.
• In a recent small, randomized, double-blind, controlled trial, investigators randomized healthy volunteers to receive 30 ml/kg of either 0.9% NS or LR. The authors report no statistical difference in the mean serum lactate when comparing LR to 0.9% NS.

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Many elderly patients have thin skin making suture repair of lacerations difficult. Consider using Steri-Strips™ in combination with sutures to close fragile skin tears.

1. Apply Steri-Strips™ perpendicular to the wound in order to approximate skin edges.

2. Place sutures through both the applied Steri-Strips™ and skin and knot the suture.

This technique will help prevent the suture from tearing the skin as the tension of the suture will be distributed across the surface area of the Steri-Strips™.

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• Migraine diagnosis should only be made after other serious intracranial diagnoses have been ruled out.
• Pediatric migraine is a difficult diagnosis to make before the age of 7 years, due to communication difficulties
• Avoid opiates and barbiturates. They have not proven to be effective, and have been shown to decrease the effectiveness of future triptan treatments. 
• First line treatment for mild to moderate migraines is acetaminophen and/or NSAID's.  The addition of caffeine, has been shown to potentiate the analgesic effects of both.
• First line treatment for moderate to severe migraines is triptans.
• Most pediatric migraines presenting to the ED, are severe migraines that have failed the above abortive home treatments and have persisted for 24+ hours.  These patients often require intravenous therapy.
• Dopamine receptor antagonist, specifically Prochlorperazine, 0.15mg/kg, 10mg max, has demonstrated the greatest effectiveness. Consider administration with diphenhydramine, 1mg/kg, 50mg max to prevent dystonic reactions.
• Concomitant dexamethasone, 0.6mg/kg, 20mg max administration has been shown to decrease acute recurrence.
• If prochlorperazine fails, other alternatives include Sumatriptan, 5-20mg IN, 50-100mg PO and lidocaine, 0.5mL of 4% solution IN.
• IVF hydration, and reduction of light and sound stimuli may be helpful.

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 A 68 year old male presents to the ED complaining of weakness to his legs. He states today his yard chores took him over 2 hours to complete instead of the usual 15-20 minutes due need to take frequent breaks for rest due to leg pain. He denied any chest pain or shortness of breath. Past medical history included hypercholesteremia, HTN,  and CAD. He is taking aspirin and recently started on rosuvastatin.

His physical exam was unremarkable.

Results showed normal EKG and CBC. Bun was 70, Creatinine was 3.4, and CPK of 1025.

This patient has statin induced rhabdomyolysis and acute renal failure.

Take Home Points:

• Rhabdomyolysis is characterized by muscle necrosis which causes the release of myoglobin into the bloodstream.
• Clinical manifestations can range from asymptomatic elevation of CPK to life-threatening cases with extremely high CPK levels, electrolyte imbalance, and acute renal failure.
• Classic triad is: muscle aches and pains, weakness, and tea-colored urine.
• Numerous recreational drugs, pharmaceuticals, and toxins can alter myocyte function. Ethanol, statins, and cocaine in particular have high risk to cause rhabdomyolysis.
• 50% of cases of statin-induced-rhabdomyolysis were due to drug interactions.

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Kohler’s disease

Osteonecrosis of the tarsal navicular bone

Affects children ages 4 to 7

               4x more likely in males

Can be painless or present with arch/midfoot pain and a limp (usually activity related)

               Usually unilateral but can be bilateral (in up to 25%)

PE: Tenderness to palpation over the length of the arch esp the medial navicular

Swelling, warmth, redness

               -Can be misdiagnosed as an infection

X-ray: Sclerosis, collapse/flattening or fragmentation of navicular

Treatment: Walking boot or short leg cast

http://www.texasfootdoctor.org/images/kohlers%20xray.jpg

Various intial doses of naloxone (0.4 to 2 mg) are administered to reverse the signs and symptoms of opioid toxicity. However, there is limited data regarding the duration of action of naloxone is correlated to the administered dose.

A recently published retrospective study investigated whether initial naloxone doses (IV), low-dose (0.4 mg) vs. high-dose (1-2 mg), lead to different time to recurrence of opioid toxicity.

Study sample: 274 patient screened but 84 patients were included.

1. Low-dose naloxone (0.4 mg IV): 42
   • Mean age: 50
   • History of opiod/heroin use: 33 (78.6%)
   • Positive opioid/opiate on drug screening: 27 (64%)
   • Median time to repeat naloxone dose: 72 min (IQR: 46 - 139)
   • 12 patients (29%) required continuous naloxone infusion

2. High-dose naloxone (1 - 2 mg IV): 42

• Mean age: 48
• History of opiod/heron use: 32 (76.2%)
• Positive opioid/opiate on drug screening: 26 (62%)
• Median time to repeat naloxone dose: 77 min (IQR: 44 - 126)
• 17 patients (41%) required continuous naloxone infusion

Higher rate of adverse effects (withdrawal symptoms - vomiting, agitation, tachycardia, etc.) were observed in high-dose group (41% vs. 31%) but this was not statistically signficant. 

Conclusion:

1. High-dose naloxone (1 - 2 mg) does not result in longer duration of reversal of opioid toxicity.
2. Duration of opioid toxicity reversal by naloxone administration were similar to previously reported duration of action of naloxone (30 to 90 min).
3. Note: there are several lmitations to the study study including retrospective design - documentation issues, small sample size, patient selection - patients were included if positive response to naloxone was observed, unknown opioid exposure, variable dosing in high-dose group (1 to 2 mg vs. 0.4 mg) and naloxone was given via IV only.   

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Critical Post-Arrest Interventions

• Critical interventions to optimize neurologic outcome in the post-cardiac arrest patient include optimizing hemodynamics, preventing lung injury, maintaining normal O2 and CO2 tensions, targeted temperature management, and treating the underlying cause of the arrest.
• Current guidelines recommend the following:
  • Target MAP > 70 mm Hg with IVFs, vasopressors, and inotropes.
  • Use a low tidal volume strategy of 6 to 8 ml/kg predicted body weight.
  • Decrease FiO2 to maintain SpO2 94% to 97%.
  • Adjust RR to maintain PaCO2 35 to 45 mm Hg
  • Initiate TTM with the goal temperature between 32 to 36^o C

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Is there an association between pulmonary aspiration, vomiting or any serious adverse event and the preprocedural fasting time?

The odds ratio of any adverse event did not increase significantly with each additional hour of fasting duration for both solids and liquids. 

The guidelines set by the American Society of Anesthesiology for fasting include a minimum of 2 hours for clear liquids, 4 hours for breast milk, 6 hours for formula and light meals and 8 hours for solid meals containing fatty foods or meat.

This was a secondary analysis of a multicenter prospective cohort study of children 0-18 years who received procedural sedation in 6 Canadian pediatric emergency departments from 2010-2015.  6183 children were included with 99.7% meeting ASA 1 or 2 categories.  2974 patients did not meet the American Society of Anesthesiology fasting guidelines for solids and 510 patients did not meet the fasting guidelines for liquids.  The overall incidence of adverse events was 11.6%.  There were no cases of pulmonary aspiration.  There was a total of 717 adverse events.  315 events were vomiting.  Oxygen and vomiting were the most common adverse events. 

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The highly-awaited PARAMEDIC2 trial results are in:

• Multicenter, double-blinded, randomized controlled trial of prehospital OHCA care
• 1mg IV epinephrine vs saline placebo, every 3-5 minutes
• 8014 OHCA patients over the age of 16 (excluded pregnant patients, anaphylactic and asthmatic cardiac arrests)
• Primary outcome: 30 day survival
• Secondary outcomes: 
  • Survival to hospital admission
  • ICU and hospital LOS
  • Survival to hospital discharge and at 3 months
  • Neurologic outcomes at hospital discharge and at 3 months, "favorable" if mRS≤3
• Results: 
  • Higher 30 day survival in Epi group (3.2 vs 2.4%, unadj OR 1.39; 95% CI 1.06 to 1.82; P=0.02)
  • No difference in ICU or hospital LOS
  • No difference in favorable neurologic outcomes at discharge or 3 month
  • Worse neurologic outcomes in the epinephrine survivors (mRS 4 or 5 in 31% of epi group vs. 17.8% of placebo)

Interestingly, the authors also queried the public as to what mattered to them most: 

Bottom Line:

• As has been demonstrated in previous studies, use of bolus-dose epinephrine results in increased rates of ROSC. 
• This survival comes with the trade-off of worsened neurologic function, a condition not in a majority of patients' personal wishes.
• Epinephrine "1mg every 3-5 minutes'" should no longer be the dogma of OHCA resuscitation.

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Exertional Heat Stroke (EHS)

With football preseason starting across the country, it is important to review this topic

EHS is a medical emergency resulting from progressive failure of normal thermoregulation

EHS has a high mortality

               -2^nd most common cause of death in football players

History and Exam

Hyperthermia/Core temperature greater than 40°C (104°F)

Initial profuse sweating with eventual cessation of sweating with hot, dry skin

CNS dysfunction – disorientation, confusion, dizziness, inappropriate behavior, difficulties maintaining balance, seizures, coma

Other: Tachycardia/hyperventilation, fatigue, vomiting, headache

Multi-organ involvement: CNS, cardiac damage, renal failure, hepatic necrosis, muscle (rhabdomyolysis), GI (ischemic colitis), heme (DIC), ARDS

The single most important thing you can do on the field is recognize this entity. Early recognition leads to earlier initiation of treatment which is life saving.

Rapid cooling is key. This is often stated but what this means is whole body immersion in ice water. This should be available and ready for all summer practices.

The temperature needs to be lowered to below 39°C (102°F)

Also consider a cooling blanket, fanning, ice to body

DO NOT put them on ambo without initiating cooling!!!

Sustaining heat injury predisposes to subsequent heat related injury

• Anticoagulation is the mainstay for treatment of acute cerebral venous thrombosis (CVT) to prevent clot propagation, recanalize occluded veins and sinuses, and prevent new venous thrombosis.
• A recent meta-analysis of 4 RCTs compared the efficacy and safety of low molecular weight heparin (LMWH) vs. unfractionated heparin (UFH) for the treatment of CVT.
• All studies were small, with 20 to 66 patients each.
• Treatment with LMWH compared with UFH had similar mortality (OR 0.21; 95% CI 0.02-2.44; p=0.21) and disability (OR 0.5; 95% CI 0.11-2.23; p=0.36). 

Bottom Line: LMWH appear to be similar in efficacy and safety compared with UFH for the management of CVT.

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Respiratory alkalosis is the most common acid-base disturbance in acute severe asthma.

Lactic acidosis is also extremely common, developing in up to 40%. This may be related to:

- tissue hypoxia

- increased respiratory muscle usage related to work of breathing

- beta agonist therapy

The first report of beta agonist administration associated with hyperlactatemia was in 1981 in patients treated for preterm labor with terbutaline. Since then, numerous case reports and studies have linked IV and inhaled beta agonist administration with the development/worsening of lactic acidosis in severe asthmatics in the ICU and in the ED.

The exact mechanism is unclear, but is thought to be related to adrenergic stimulation leading to increased conversion of pyruvate to lactate.

In a study published in Chest in 2014, investigators evaluated plasma albuterol levels and serum lactate levels, as well as FEV1.

They found plasma albuterol levels correlated with lactate concentration and maintained significant association after adjusting for asthma severity (suggesting the association was independent of work of breathing/respiratory muscle usage).

Furthermore, several reports have suggested that dyspnea may improve in patients with elevated lactate and acidosis after beta agonists are withheld.

Take Home Points:

- Beta agonist therapy may contribute to lactic acidosis.

- Lactic acidosis may contribute to respiratory distress.

- In patients on prolonged, high-dose beta agonist therapy, consider checking a serum lactate periodically. If elevated, consider whether worsening lactic acidosis is contributing to respiratory distress and contemplate transitioning to less frequent treatments.

-Patients with severe asthma exacerbation and elevated serum lactate must have thorough evaluation for true tissue hypoxia/hypoperfusion. **Beta agonist associated hyperlactatemia should be a diagnosis of exclusion.**

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Is your older patient hard of hearing (HoH)? Instead of shouting, get a stethoscope. Put the ear buds in your patient's ears and talk into the bell. It is a hearing amplifier you carry with you.

Bonus pearl: If you use the disposable stethoscopes, then the patient can keep it in their room and use it whenever anyone wants to talk to them.

• IDSA/SHEA recently released a guideline update for the management of Clostridium difficle infections
• Discontinue inciting antibiotic therapy as soon as possible
• Metronidazole is no longer considered first line therapy for C. difficle infection
• Treatment course for 10 days unless initial fulminant or recurrence requiring vancomycin taper
• Remember: Vancomycin IV does not cross into the GI tract and cannot be used to treat C. difficile

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Delayed Onset Muscle Soreness (DOMS), aka “muscle fever”

Muscle pain and weakness following unfamiliar exercise

Occurs after high force, novel (unaccustomed) eccentric muscle contractions

               Occasionally isometric in an extended position

Eccentric exercise – controlled elongation

Slowly lowering yourself to start position doing pullups for example

Time of onset

Begins 6 to 12 Hours after exercise, Peaks 2-3days post and resolves in 5-7 days

               Speed of onset and severity are often related

How do you know if you have it?

Much like the flu, you know it when you have it. The simple act of getting out of a car, sitting down or walking down stairs is excruciatingly painful.

Cause:

Exact cause is unknown. Thought to be due to sarcolemma damage leading to intra cellular calcium release and activation of proteolytic enzymes. Creatine kinase leaks from muscle cells into plasma attracting inflammatory cells.

Treatment:

Best treatment is prevention: Repeated bout effect – a bout of eccentric or isometric exercise can prevent DOMS from the same exercise for 4-12 weeks.

               Stretching before exercise has not been shown to be effective prevention

Other modalities: rest, ice, heat, massage, electrical stimulation

Take home:

Eccentric exercises or novel activities should be introduced progressively over a period of 1 or 2 weeks at the beginning of the sporting season or the start of a new, novel exercise routine. For example, not starting the Insanity day one workout without “pretraining.” This will reduce the level of physical impairment and/or training disruption and lead to gains with much less pain.

Elevated transaminases are found in both rhabdomyolysis and delayed acetaminophen (APAP) toxicity. Establishing the cause of elevated transaminase can be difficult when there is unclear history of acetaminophen ingestion.

A retrospective study of patients with delayed acetaminophen toxicity or rhabdomyolysis from 2006 to 2011 was recently published.

The authors compared AST/ALT, CK/AST and CK/ALT ratio of 

• 160 in the rhabdomyolysis group
• 68 in the acetaminophen overdose (all)
• 29 in the delayed acetaminophen overdose group

Results

AST/ALT ratio

• Rhabdomyolysis group: 1.66
• APAP overdose (all): 1.38
• Delayed APAP overdose: 1.3

CK/AST ratio

• Rhabdomyolysis group: 21.3
• APAP overdose (all): 5.49
• Delayed APAP overdose: 3.8

CK/ALT ratio

• Rhabdomyolysis group: 37.1
• APAP overdose (all): 5.77
• Delayed APAP overdose: 5.03

Conclusion

• Significantly higher ratio of AST/ALT, CK/AST and CK/ALT were found in rhabdomyolysis patients than delayed APAP overdose patients.
• These finding are based on small study population and need further validation/research before clinical application.