Infective endocarditis (IE) The most common overall cause of IE is Streptococcus viridans. The most common cause of IE in injection drug users is Staphylococcus aureus. The most common cause of IE in patients with prosthetic valves is also Staphylococcus species; in the first two months postop coag-negative Staphylococcus predominates, and after that the most common causes are Staphylococcus aureus, Streptococcus viridans, and enterococcus. In treating IE of prosthetic valves and/or in injection drug users, the addition of rifampin to the standard regimen of nafcillin/vancomycin + gentamycin is often recommended in order to add additional gram positive coverage.

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.

Recognize the signs of venous air embolism when inserting a central venous catheter * Although rare, a feared complications of CVC insertion is venous air embolism (VAE) * Conditions that increase the risk of VAE are detachment of catheter connections, failure to occlude the needle hub during insertion, hypovolemia, and upright positioning of the patient * Clinically, VAE presents with acute dyspnea, cough, chest pain, altered mental status, tachypnea, tachycardia, and/or hypotension * Treatment includes placing the patient in a left lateral decubitus position, reverse Trendelenburg, and providing 100% oxygen via NRB * Also consider hyperbaric oxygen therapy * Aspiration of air, as recommended in some textbooks, is rarely successful Reference: Mirski MA. Lele AV. Fitzsimmons L. Toung TJ. Diagnosis and treatment of vascular air embolism. Anesthesiology 2007;106(1):164-77.

Use plateau pressure, rather than peak inspiratory pressure, as a means of assessing the risk of barotrauma * One mechanism (of many) by which mechanical ventilation can induce acute lung injury in patients with ARDS is overdistention of the alveoli * 2 common parameters used to assess airway pressures are plateau pressure (Pplat) and peak inspiratory pressure (PIP) * Pplat approximates small airway and alveolar pressures more closely than PIP * ARDSnet trial demonstrated a reduction in the number of ventilator days and mortality when Pplat was maintained < 30 cm H2O. References: 1. ARDS Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. NEJM 2000;342:1301-8. 2. Marcucci L, ed. Avoiding common ICU errors. Philadelphia; Lippincott Williams & Wilkins; 2007:275-6.

Be alert for cyanide toxicity when using sodium nitroprusside * Toxicity from sodium nitroprusside can be seen in as little as 2-4 hours with rates > 4.0 mcg/kg/min * Patients with hepatic and renal dysfunction are at greatest risk * Clinical signs of toxicity include altered mental status (agitation, restlessness), tachycardia, ventricular arrhythmias, and eventually hypotension * The classic anion-gap metabolic acidosis is a pre-terminal event - do not wait for this to develop to raise suspicion of toxicity! Reference: Marcucci L, ed. Avoiding common ICU errors. Philadelphia; Lippincott Williams & Wilkins; 2007:148-9.

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)

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

Helpful clues to distinguishing pericarditis vs. STEMI Pericarditis: PR depression in multiple leads, PR elevation > 2 mm in aVR; friction rub (specific though not sensitive) Remember that PR depression mainly only shows up in viral pericarditis, not other types STEMI: horizontal or convex upwards (like a tombstone) STE, ST depression in any lead aside from aVR and V1, STE in III > II

Calcium's main effect on the ECG appears to be on the duration of the ST segment, such that: 1. Hypercalcemia shortens the ST segment, producing also a short QTc. 2. Hypocalcemia prolongs the ST segment, producing also a long QTc. As an aside, there are only three conditions in which a short QTc is typically noted: hypercalcemia, digitalis toxicity, and a recently described syndrome that causes sudden death--"the short QT syndrome" (in which the QTc may be < 300ms...that's REALLY short!). As another aside, there are only two conditions that prolong the QTc via prolongation of the ST segment--hypocalcemia and hypothermia.

D-Dimer levels are known to be elevated in pregnancy. But how high is too high and can this test be used in the workup of VTE in pregnant patients?

Recent literature indicates that D-dimer levels in each of the three trimesters are approximately 39% higher: 700, 1000, and 1400 ng/dL for each trimester (normal cutoff 500 ng/dL). So, figure out what trimester your patient is in and use the corresponding D-Dimer level for that trimester.

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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.

Hydrofluoric acid is a weak acid used primarily in industrial applications for glass etching and metal cleaning/plating. It is contained in home rust removers. Although technically a weak acid, it is very dangerous and burns can be subtle in appearance while having severe consequences.

Wilkes G. Hydrofluoric Acid Burns. Jan 28, 2010. 
http://emedicine.medscape.com/article/773304-overview

• 2 mechanisms that cause tissue damage*
  • corrosive burn from the free hydrogen ions
  • chemical burn from tissue penetration of the fluoride ions
• Clinical features*
  • Cutaneous burns - absent findings to white-blue appearance
  • Pulmonary edema
  • Hypocalcemia, hyperkalemia, hypomagnesemia
• Treatment*
  • Decontaminate by irrigation with copious amounts of water.
  • With any evidence of hypocalcemia, immediately administer 10% calcium gluconate IV.
  • Cutaneous burns:
    • Apply 2.5% calcium gluconate gel to the affected area. If the proprietary gel is not available, constitute by dissolving 10% calcium gluconate solution in 3 times the volume of a water-soluble lubricant (eg, KY gel). For burns to the fingers, retain gel in a latex glove.
    • If pain persists for more than 30 minutes after application of calcium gluconate gel, further treatment is required. Subcutaneous infiltration of calcium gluconate is recommended at a dose of 0.5 mL of a 5% solution per square centimeter of surface burn extending 0.5 cm beyond the margin of involved tissue (10% calcium gluconate solution can be irritating to the tissue).
      • Do not use the chloride salt because it is an irritant and may cause tissue damage.

*Extracted from emedicine article.

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Question

An alcoholic patient presents with a cough, fever, and very foul smelling breath (worse than usual)

What's the diagnosis? And what are the risk factors?

 

 

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