UMEM Educational Pearls - Critical Care

Mechanical Ventilation "Knobology" - Oxygenation -FiO2 and PEEP are used to improve oxygenation in the ventilated patient -Immediately following intubation, start with an FiO2 of 100% -Increase PEEP by 2-3 cm H2O every 10-15 minutes to achieve the desired saturation -As you titrate PEEP, have respiratory therapy provide you with plateau pressures (maintain Pplat < 30) Mike

Fungal Infections * Fungal isolates are an increasingly common source of bloodstream infections in critically ill patients * Mortality ranges from 20% to 60% in some series * 50% are non-albicans species (C.glabrata, C.parapsilosis, C.tropicalis, and C. krusei) * Risk factors include ventilated patients, TPN, high APACHE scores, abdominal surgery, and prolonged ICU stays * Think of fungal infections in the septic patient with hypothermia and bradycardia * Newer antifungal agents such as voriconazole and caspofungin have improved efficacy against n

Subclavian central venous access * Many consider the subclavian to be the preferred route for central venous access * Approximately 5-6% of subclavian's are associated with misdirection of the catheter tip into the internal jugular * Directing the J-tip of the guidewire caudally significantly reduces the incidence of malpositioning Reference: Tripathi M, et al. Direction of the J-Tip of the guidewire, in seldinger technique, is a significant risk factor in misplacement of subclavian vein catheters: a randomized, controlled study. Anesth Analg 2005;100:21-4.

Life- or Limb-saving Escharotomy * At some point in your career you may have to perform an emergent escharotomy to safe a life or limb * Deep thickness circumferential chest burns act like a straight jacket and impair respiration * Circumferential limb burns act like a tourniquet and impairs both venous output and arterial input resulting in ischemia * Limb escharotomy should be performed as soon as pulses diminish - do not wait for them to disappear * The picture illustrates the incision lines for escharotomy (note the bold lines highlight the importance of going across any involved joint)

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In the absence of contraindications, keep the head of the bed elevated 30 degrees for intubated patients * Mechanical ventilation places patients at risk for ventilator-associated pneumonia (VAP) * ICU mortality for VAP ranges from 30% to 70% * Elevating the head of the bed has been shown to decrease the frequency of VAP Reference: Dodek P, Keenan S, Cook D, et al. Evidence-based clinical practice guideline for the prevention of ventilator-associated pneumonia. Ann Intern Med 2004;141:305-13.

Start antibiotics ASAP in patients with septic shock * For patients with septic shock, start antibiotics within the first hour * For each additional hour that antibiotics are delayed, survival decreases by 7%-8%! * Once you address the ABC's, obtain appropriate cultures, and hang the antimicrobials * Make sure you are providing effective antimicrobials (take a look at the patient's history to see if they have resistant bugs) Reference: Kumar A, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in septic shock. Crit Care Med 2006;34:1589-96.

Obtain serial lactate levels in ED patients with infection * Elevated serum lactate is associated with an increased risk of death in critically ill patients with infection * An initial lactate level > 4.0 mmol/l is significant and, in some series, is associated with a mortality of approximately 40% * Obtain serial venous lactate measurements every 3-4 hours * If serial levels remain > 4 mmol/l, or rise, be more aggressive with resuscitation Reference: Trzeciak S, et al. Serum lactate as a predictor of mortality in patients with infection. Inten Care Med 2007;33:970-7.

Critical care of patients with HIV/AIDS - Lactic Acidosis * Lactic acidosis can be a life-threatening complication of HAART - mortality as high as 77% * It can occur with any of the nucleoside/nucleotide reverse transcriptase inhibitors (most common are didanosine and stavudine) * Common presenting symptoms include abdominal pain, nausea, vomiting, myalgias, and elevation of transaminases * In patients with these symptoms check a lactate -> a value > 5 mmol/L is considered life-threatening * Treatment is supportive care with removal of the offending medication * In anecdotal reports, L-carnitine, thiamine, and riboflavin may reverse toxicity Reference: Morris A, Masur H, Huang L. Current issues in the critical care of the human immunodeficiency virus-infected patient. Crit Care Med 2006;34:42-9.

TRALI - Transfusion Related Acute Lung Injury * TRALI has now emerged as the primary cause of transfusion-associated mortality, surpassing infectious complications and ABO mismatch * TRALI is defined as new ALI in a patient receiving, or having just received (within the past 6 hours), a blood product transfusion * All plasma-containing products have been implicated (FFP and platelets are the top offenders) * Clinically, patients present with dyspnea, tachypnea, and hypoxia * CXR findings are consistent with noncardiogenic pulmonary edema * There is no unique treatment for TRALI; most patients have resolution within 96 hours * AVOID diuretics as these patients are often volume depleted Reference: 1. Looney MR. Newly recognized causes of acute lung injury: transfusion of blood products, severe acute respiratory syndrome, and avian influenza. Clin Chest Med 2006;27:591-600.

Make sure the Cordis is the right size when floating a pacing wire * At some point in your career, you may need to "float" a transvenous pacing wire * When inserting the wire, you need to make sure you have the right size Cordis * In general, a pacing wire should be inserted through a 6F Cordis (0.198 mm) * Many introducer kits have a 7.5F Cordis (0.2475mm) that is used for insertion of a PAC * Blood loss, infection, and air embolism are risks that can occur when the Cordis catheter used is too large Reference: 1. Marcucci L, ed. Avoiding common ICU errors. Philadelphia; Lippincott Williams & Wilkins; 2007:275-6.

Critical Illness Neuromyopathy (CINM) * CINM is the most common peripheral neuromuscular disorder encountered in the ICU * CINM may contribute to delayed weaning and prolonged ventilation * Risk factors for CINM include SIRS/MODS, sepsis, and hyperglycemia (corticosteroid use still controversial) * Current mainstay of management is directed at prevention * EM take home point -> Judicious use of medications associated with the development of CINM (aminoglycosides, neuromuscular blocking agents) Reference: De Jonghe B, Lacherade JC, Durand MC, et al. Critical illness neuromuscular syndromes. Crit Care Clin 2007;23:55-69. (compliments of Dr. Winters)

Oxygenation goals

• In recent pearls we have talked about 'lung protective' ventilation strategies to reduce volutrauma, barotrauma, and oxygen toxicity.
• Using 'lung protective' strategies, such as low tidal volumes, results in higher levels of CO₂ and a lower pH.  These are tolerated in favor of lower and safer alveolar pressures.
• In addition to higher pCO₂ values and lower pH, oxygenation goals are slightly lower than conventional teaching.
• In these patients, you want to maintain S_pO₂ > 88% and P_aO₂ > 55 mm Hg.

Adrenal insufficiency (AI) can be a life-threating condition and is classified as primary (failure of the adrenal gland) or secondary (failure of hypothalamic- pituitary axis).

Common causes of primary adrenal insufficiency include autoimmune destruction, infectious causes (TB and CMV), or interactions with drugs (e.g., anti-fungals, Etomidate, etc.). Secondary causes are usually due to abrupt withdrawal of steroids after chronic use, although sepsis and diseases of the hypothalamus or pituitary (e.g., CVA) may occur.

Signs and symptoms include fatigue, weakness, skin pigmentation, dizziness, abdominal pain, and orthostatic hypotension; it should be suspected with any of the following: hyponatremia, hyperkalemia, hypoglycemia, hypercalcemia, low free-cortisol level, and hemodynamic instability despite resuscitation.

Treatment:
• Correct underlying the disorder
• Resuscitation and hemodynamic support
• Correct hypoglycemia and electrolyte abnormalities
• Treat with hydrocortisone, cortisone, prednisone, or dexamethasone +/- fludrocortisone (Note: dexamethasone is attractive choice in the ED because it will not interfere with ACTH stimulation test)

 

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It is well documented that when left to our own respiratory devices we will consistently over-ventilate patients presenting in cardiac arrest (1). A simple and effective method of preventing these overzealous tendencies is the utilization of a ventilator in place of a BVM. The ventilator is not typically used during cardiac arrest resuscitation because the high peak-pressures generated when chest compressions are being performed cause the ventilator to terminate the breath prior to the delivery of the intended tidal volume. This can easily be overcome by turning the peak-pressure alarm to its maximum setting. A number of studies have demonstrated the feasibility of this technique, most recently a cohort in published in Resuscitation by Chalkias et al (2). The 2010 European Resuscitation Council guidelines recommend a volume control mode at 6-7 mL/kg and 10 breaths/minute (3).

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Identifying patients at risk of hypotension during intubation is not always straight forward. The prevalence of peri-intubation hypotension in the Emergency Department has been demonstrated to be approximately 20%.¹ And while certain variables increase the likelihood of peri-intubation hypotension (ex. Shock index> 0.80), no single factor predicts it accurately enough to be used at the bedside.² In the majority of patients undergoing intubation, clinicians should be prepared for peri-intubation hypotension with either vasopressor infusions or push dose pressors.

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While lung protective ventilatory strategies have long been accepted as vital to the management of patients undergoing mechanical ventilation, the translation of such practices to the Emergency Department is still limited and inconsistent.

Fuller et al employed a protocol ensuring lung-protective tidal volumes, appropriate setting of positive end-expiratory pressure, rapid weaning of FiO2, and elevating the head-of-bed. The authors found that the number of patients who had lung protective strategies employed in the Emergency Department increased from 46.0% to 76.7%. This increase in protective strategies was associated with a 7.1% decrease in the rate of pulmonary complications (ARDS and VACs), 14.5% vs 7.4%, and a 14.3% decrease in in-hospital mortality, 34.1% vs 19.6%.

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Question

In a study of alarms from 77 monitored ICU beds over the course of a month at the University of California, San Francisco, false alarms were common. Accellerated Ventircular Rhythms (AVRs) made up roughly one third of the alarms, and of the more than 4,361 AVRs, 94.9% were false while the remaining 5.1% did not result in a clinical action.

While this study had a majority of patients in the Med/Surg ICUs, a minority were from the cardiac and neurologic ICUs giving it some broad applicability. This study adds to the literature indicating there are subsets of alarms which may not be necessary or which may require adjustment to increase specificity.

Suba S, Sandoval CS, Zegre-Hemsey J, et al. Contribution of Electrocardiographic Accelerated Ventricular Rhythm Alarms to Alarm Fatigue. American Journal of Critical Care. 2019; 28(3):222-229

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Question

Don’t miss the injecting drug users with botulism!

Wound botulism presents as descending paralysis when Clostridium botulinum spores germinate in anaerobic necrotic tissue. There have been hundreds of cases in the last decade, but it is poorly reported outside of California.

Black tar heroin and subcutaneous injection (“skin popping”) carry the highest risk, but other injected drugs and other types of drug use suffice. C botulinum spores are viable unless cooked at or above 85°C for 5 minutes or longer and this is not achieved when cooking drugs. 

Early administration of botulism anti-toxin (BAT) not only saves lives but can prevent paralysis and mechanical ventilation. An outbreak of 9 cases between September 2017 and April 2018 cost roughly $2.3 million, in part because patients didn’t present on average until 48 hours after symptom onset and it took an additional 2-4 days before the true cause of their respiratory depression and lethargy were understood. One patient died.

PEARL: talk to your injecting drug users about the symptoms of botulism: muscle weakness, difficulty swallowing, blurred vision, drooping eyelids, slurred speech, loss of facial expression, descending paralysis, and difficulty breathing. Consider botulism early in your patients who inject drugs but who do not respond to naloxone or who exhibit prolonged symptoms. Testing at the health department is performed with mouse antibodies to Botulism Neurotoxin (BoNT) combined with the patient’s serum.

 

 

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Torsades de pointes and QT prolongation Associated with Antibiotics

 

Methods

The authors queried the United States FDA Adverse Event Reporting System (FAERS) from 01/01/2015 to 12/31/2017 for reports of Torsade de points/QT prolongation (TdP/QT).

Reporting Odd Ratio (ROR) was calculated as the ratio of the odds of reporting TdP/QTP versus all other ADRs for a given drug, compared with these reporting odds for all other drugs present in FAERS

Results

FAERS contained 2,042,801 reports from January 1, 2015 to December 31, 2017. There were 3,960 TdP/QTP reports from the study period (0.19%).

 

Macrolides               ROR 14 (95% CI 11.8-17.38)

Linezolid                  ROR 12 (95% CI 8.5-18)

Amikacin                 ROR 11.8 (5.57-24.97)

Imipenem-cilastatin ROR 6.6 (3.13-13.9)

Fluoroquinolones   ROR 5.68 (95% CI 4.78-6.76)

 

Limitations:

These adverse events are voluntary reports

There might be other confounded by concomitant drugs such as ondansetron, azole anti-fungals, antipsychotics.

 

Bottom Line:

This study confimed the previously-known antibiotics to be associated with Torsades de pointes and QT prolongation (Macrolides, Linezolid, Imipenem and Fluoroquinolones). However, this study  found new association between amikacin and Torsades de pointes/QT prolongation.

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Rapid Assessment of the RV on Bedside Echo

There are several causes of acute RV dysfunction resulting in a patient presenting to the ER with unstable hemodynamics. Some of these include acute cor pulmonale, acute right sided myocardial infarction and acute submassive or massive pulmonary embolism. While bedside assessment of the LV function is often performed by the ED physician, simultaneous evaluation of the RV can provide crucial information that can help guide therapeutic decisions to prevent worsening of the patient’s clinical condition. A rough guideline to determine RV size and function is below using the apical 4 chamber view.

Normal RV size :            <2/3 the size of the LV

Mildly enlarged RV :       >2/3 the size of the LV, but not equal in size

Moderately enlarged RV:  RV size = LV size

Severely enlarged RV:      RV size > LV size

Patients who are found to have RV dilation should be given fluids in a judicious fashion as the RV is not tolerant of fluid overload. Early diagnosis of the cause of acute RV failure should be sought to guide definitive therapy, but early institution of inotropic support should be considered. Frequent reassessments of biventricular function during resuscitation should be performed.

 

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