UMEM Educational Pearls - Critical Care

Category: Critical Care

Title: Carbapenem Resistant Organisms are HERE

Keywords: Carbapenem Resistant Organisms, CRE, Pseudomonas, Infectious Diseases, Antimicrobial Stewardship (PubMed Search)

Posted: 5/15/2014 by John Greenwood, MD (Emailed: 5/20/2014) (Updated: 5/20/2014)
Click here to contact John Greenwood, MD

 

Carbapenem Resistant Organisms are HERE

 

We've all heard Dr. Bryan Hayes warn us that, "Vanc & Zosyn is NOT the Answer for Everything" but things just got a little more serious, on a whole 'nother level...

Within the past few months, 2 cases of NDM-producing carbapenem-resistant pseudomonas have been reported in the area - one in Delaware and one in Pennsylvania.  Previously, the only reported cases were found in Europe.  

It's important for EM physicians to be aware of carbapenem resistant organisms and infections because:

  • They have been independently associated with an increase in mortality
  •  Are increasing in frequency around the world
  • Are a major threat to our antimicrobial armamentarium

Risk factors for carbapenem resistance 

  • Stem cell transplant patients
  • History of mechanical ventilation
  • Recent ICU stay
  • Previous exposure to antibiotics

Antimicrobial options

Few treatment options are currently available for carbapenem resistant organisms.  

  • Polymixins (colistimethate & polymyxin B)
  • Tigecycline
  • Fosfomycin
  • Some aminoglycosides (amikacin, gentamicin, & tobramycin)

Appear to have retained some in vitro activity against these organisms, but are generally used as, "drugs of last resort". 

What should you do about it?

Know it exists, take a good history, & know your local antibiogram.  Prior to selecting a broad spectrum antimicrobial regimen, try to obtain previous antimicrobial culture data for patients with resistant organism infectious risk factors.

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Prior literature has demonstrated the safety and feasibility of placing subclavian lines with ultrasound guidance; here's a link to a short educational video describing the technique. 

The literature has been varied, however, as to which approach is best for venous cannulation with ultrasound; the supraclavicular (SC) or infraclavicular (IC) approach (see references below)

A recent study evaluated both approaches in healthy volunteers in order to determine which approach is superior for cannulation using ultrasound.

98 patients were prospective evaluated by Emergency Medicine physicians with training in ultrasound. In each patient, both SC and IC views were evaluated on both the left and right sides; each view was given a grade for ease of favorability (no patients were actually cannulated)

Overall, it was found that the SC view was significantly more favorable compared to the IC view; the right SC was non-significantly preferred compared to the left SC.

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Category: Critical Care

Title: High Flow Nasal Cannula

Keywords: HFNC, vapotherm, high flow, nasal cannula, hypoxemia (PubMed Search)

Posted: 5/7/2014 by Feras Khan, MD (Updated: 7/22/2024)
Click here to contact Feras Khan, MD

High Flow Nasal Cannula

What is it?

  • High flow nasal cannula has been used in pediatrics for some time now
  • It can be used in adults as well
  • It is a simple nasal cannula setup with larger cannula sizes in both nares
  • It is heated, humidified oxygen
  • You can control your oxygen level and flow of oxygen

Benefits

  • Small amount of PEEP provided to the patient (estimated 5-7 cm H20)
  • Improves oxygenation (more reliable oxygenation than a non-rebreather face mask)
  • Can provide some alveolar recruitment
  • Increases FRC (functional residual capacity)
  • Pharyngeal dead space washout

Who to use it on

  • Acute hypoxemic respiratory failure
  • Pre-intubation (can place before and during intubation in patients who have low oxygen saturation)
  • Post-extubation
  • Palliative care (DNI patients)

How to set it

  • Flow rates: 0-60 L/min
  • Spontaneously breathing patient with mild-moderate hypoxemia/respiratory distress:

            -15-30 L per minute

            -100% oxygen (wean as tolerated)

            -temp 35-40 C

            -when weaning decrease oxygen prior to flow

Bottom line: No evidence that it reduces intubation rates in patients with hypoxemic respiratory failure but may improve oxygenation issues while deciding on treatment options

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Antibiotic Timing in Severe Sepsis/Septic Shock

  • Though the recent ProCESS trial has questioned the utility of central hemodynamic monitoring and protocol-based resuscitation, early antibiotic administration remains paramount in the care of patients with severe sepsis/septic shock.
  • Retrospective studies have demonstrated that delays in antibiotic administration are associated with marked increases in hospital mortality.
  • Notwithstanding, delays in antibiotic administration remain all too common.
  • Ferrer et al, have just published the largest cohort to date analyzing the association of antibiotic timing to hospital mortality in patients with severe sepsis or septic shock.  The key findings include:
    • Retrospective cohort of 17,990 patients from the SSC database.
    • Hospital mortality rose linearly for each hour delay in antibiotic administration.
    • Odds ratio for hospital mortality increased from 1 to 1.52, as the delay increased from 0 to 6 hours after presentation.
  • Key Point: Antibiotic timing matters!

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Category: Critical Care

Title: Considering "The Lethal Duo" when Intubating the patient with TBI

Keywords: intubation, neurocritical care, mechanical ventilation, direct laryngoscopy, video laryngoscopy (PubMed Search)

Posted: 4/20/2014 by John Greenwood, MD (Emailed: 4/22/2014) (Updated: 4/22/2014)
Click here to contact John Greenwood, MD

 

Direct vs. video laryngoscopy in the patient with an acute TBI

Hypoxia and hypotension are considered the "lethal duo" in patients with traumatic brain injury.  In a recent randomized control trial (by our own Dr. Dale Yeatts at the Shock Trauma Center) mortality outcomes were compared between 623 consecutive patients who were intubated with either direct laryngoscopy (DL) or video laryngoscopy (VL).  Here is what they found:

1. No significant difference in mortality for all comers (Primary Outcome)
2. In the subset of patients with severe head injuries, there was:

  • A significantly higher mortality in patients with TBI if VL was used
  • A significantly longer intubation duration for VL (74 sec) than DL (65 sec)
  • A greater incidence of low oxygen saturations of 80% or less in the VL group (27 patients) than DL (15 patients) - objectively recorded data, not self reported.

There is a reasonable amount of literature that shows hypoxia and hypotension significantly contribute to morbidity & mortality in the TBI patient, and a growing body of literature that suggests intubation with VL takes longer than DL.

 

Bottom Line: When choosing a method of intubation for the TBI patient, remember the "Lethal Duo" and consider direct laryngoscopy with manual inline stabilization first.

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  • Only 50% of hemodynamically unstable patients will improve their hemodynamics in response to a fluid bolus. However, because excessive fluid administration can lead to organ edema and dysfunction, it is important to give hemodynamically unstable patients only the necessary amount of fluids to improve their hemodynamics.

  • There are two general categories of assessing a patient's response to volume administration; static and dynamic assessments (see referenced article below):

    • Static assessment (generally unreliable, but traditionally used):

      • Physical exam (dry mucus membranes, cool extremities, etc.)

      • Urine output

      • Blood pressure

      • Central venous pressure via central-line

    • Dynamic assessment (more reliable but more labor intensive)

      • Pulse Pressure Variation

      • IVC Distensibility Index

      • End-expiratory occlusion test

      • Passive Leg-Raise

  • There is no simple way to accurately determine the need for a fluid bolus however the integration of the techniques above can help the clinician make better decisions.

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Category: Critical Care

Title: How low should you go? MAP Goals in Septic Shock

Keywords: map, sepsis, septic shock, hypertension (PubMed Search)

Posted: 4/7/2014 by Feras Khan, MD (Emailed: 4/8/2014) (Updated: 4/8/2014)
Click here to contact Feras Khan, MD

How low should you go? MAP Goals in Septic Shock

Background:

  • Since Rivers’ Early-Goal Directed Therapy, a MAP of 65 mm Hg was been the standard goal for blood pressure in septic shock
  • Some studies have suggested a higher target may be better for patients with hypertension
  • Potentially less renal failure with a higher target

The Trial:

  • 776 adult patients in France; Multi-center; randomized; non-blinded
  • All patients had septic shock and on vasopressors
  • MAP was maintained for 5 days or when the patient was weaned off pressors
  • Primary outcome: Mortality at Day 28
  • High target 65-70 mm Hg vs Low target 80-85 mm Hg

Outcome:

  • No significant difference in mortality at 28 days: 36.6%  (high target) vs 34% (low target) (95 %CI; 0.84 to 1.38; P=0.57)
  • No significant difference at 90 days: 43.8% (high target) vs 42.3% (low target) (95% CI; 0.83 to 1.30; P=0.74)
  • Incidence of newly diagnosed atrial fibrillation was higher in the high-target group
  • Patients with chronic hypertension: those in the higher target group required less renal-replacement therapy
  • Significant percentage of patients in the high target group did not meet goal MAP BUT the trial mirrored actual clinical practice and allowed clinicians the ability to limit blood pressure and differences in actual MAP attained in both groups was significantly different

Bottom Line:

  • A MAP goal of 65 is just fine in most patients
  • Patients with chronic hypertension and atherosclerosis seem to benefit (less need for renal-replacement therapies) with a higher MAP: so aim higher in these patients or monitor renal function and increase MAP goals accordingly

 

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Coagulopathies in Critical Illness - DIC

  • Disseminated intravascular coagulation (DIC) is an acquired syndrome of intravascular coagulation and is commonly encountered in critically ill patients.
  • Think about DIC in the critically ill patient with oozing at vascular sites (or wounds) and the following lab abnormalities:
    • Thrombocytopenia
    • Prolonged PT and aPTT
    • Decreased fibrinogen
    • Elevated fibrin split products and D-dimer
  • Guidelines for the management of DIC are primarily based on expert opinion and include:
    • Treat the underlying condition (i.e., sepsis)
    • Transfuse platelets if < 50,000 per mm3
    • Transfuse FFP to maintain PT and aPTT < 1.5 times normal control
    • Transfuse cryoprecipitate to maintain fibrinogen levels > 1.5 g/L
  • The use of heparin remains controversial and cannot be routinely recommended.

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Category: Critical Care

Title: There appears to be NO role for iNO in ARDS

Keywords: ARDS, Nitric Oxide, acute respiratory failure, mechanical ventilation (PubMed Search)

Posted: 3/23/2014 by John Greenwood, MD (Emailed: 3/25/2014) (Updated: 3/26/2014)
Click here to contact John Greenwood, MD

 

Nitric Oxide appears to have NO role in ARDS

Background: The use of inhaled nitric oxide (iNO) in acute respiratory distress syndrome (ARDS) & severe hypoxemic respiratory failure has been thought to potentially improve oxygenation and clinical outcomes.  It is estimated that iNO is used in up to 14% of patients, despite a lack of evidence to show improved outcomes. 

Mechanism: Inhaled NO works as a selective pulmonary vasodilator which has been found to improve PaO2/FiO2 by 5-13%, but is costly ($1,500 - $3,000 per day) and increases risk of renal failure in the critically ill.

Study: A recent systematic review analyzed 9 different RCTs (N=1142) and compared mortality between those with severe (PaO2/FiO2 < 100) and less severe (PaO2/FiO2 > 100) ARDS and found that iNO does not reduce mortality in patients with ARDS, regardless of the severity of hypoxemia.


Bottom Line: Inhaled NO is an intriguing option for the treatment of refractory hypoxemic respiratory failure, however there does not appear to be a mortality benefit to justify it's high cost and potentially negative side effects.  In the ED, it is important to focus on appropriate lung protective ventilation strategies (TV: 6-8 cc/kg IBW) and maintaining plateau pressures < 30 cm H2O in the initial stages of ARDS to prevent ventilator induced lung injury while awaiting ICU admission.

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In 2001, Rivers et al. published a landmark article demonstrating an early-goal directed protocol of resuscitation that reduced mortality in septic Emergency Department patients.

Many questions have arisen throughout the years with respect to that trial; critics have complained about the overwhelming change in clinical practice based on this one single-center randomized trial.

Challenging Rivers data are the ProCESS (Protocolized Care for Early Septic Shock) investigators, who released the results from a multi-center randomized control trial of 1351 septic Emergency Department patients; the primary end-point was 60-day mortality. Click here for NEJM article.

Patients in this trial were randomized to one of three groups:

  • Protocol-based EGDT

  • Protocol-based standard (did not require central lines, inotropes, or blood transfusions

  • Usual care (no specific protocol; care was left to the bedside clinicians)

Bottom-line: The investigators did not find any difference in mortality between patients in the three groups and comment that the most important aspects of managing the septic patient may be prompt recognition and early treatment with IV fluids and antibiotics.

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Category: Critical Care

Title: Lung Ultrasound in Pulmonary Edema

Keywords: lung ultrasound, pulmonary edema, B-lines (PubMed Search)

Posted: 3/11/2014 by Feras Khan, MD
Click here to contact Feras Khan, MD

  • “B-Lines” can be seen in patients with pulmonary edema (see attached image below)
  • A “B-line” is a reverberation artifact defined by Lichtenstein as having several properties:

1.     A comet-tail artifact

2.     Arising from the pleural line

3.     Well defined

4.     Hyperechoic

5.     Long (does not fade)

6.     Erases A lines

7.     Moves with lung sliding

 

  • A large amount of B-lines is pathologic
  • These artifacts are also called “comet-tails” due to their appearance
  • One or two B-lines can be seen in dependent lung zones in normal lungs
  • AIS (Alveolar interstitial syndrome) describes a group of conditions including pulmonary edema, interstitial pneumonia, and pulmonary fibrosis that show similar findings on lung ultrasonography
  • The most common presentation of this syndrome is from cardiogenic pulmonary edema and is characterized by B-lines in multiple lung zones
  •  B lines correspond with interlobular septal thickening on CT scans, which represent pulmonary vascular congestion 

Technique

  • B-mode is used with the micro-convex (cardiac) probe scanning in at least 8 lung zones
  • Quantify the number of B-lines in each zone
  • A lung zone is considered to be “positive” when three or more B-lines are present in a longitudinal plane between two ribs
  • Two or more regions bilaterally are required to be defined as AIS
  • Bilateral diffuse B-lines have a specificity of 95% and a sensitivity of 97% for the diagnosis of pulmonary edema

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Attachments

1403111625_Fig6.1BLINESFINAL.jpg (55 Kb)



Recruitment Maneuvers for ARDS

  • Patients with ARDS who are ventilated with lung protective settings are at risk of derecruitment/collapse of lung units.
  • Recruitment maneuvers are processes that transiently increase transpulmonary pressure to open collapsed units.
  • These maneuvers can improve oxygenation and have been used in patients with ARDS and those with refractory hypoxemia.
  • The various types of recruitment methods include:
    • Airway pressure-based maneuver: a continuous positive airway pressure of 35-45 cm H2O is applied for 30-40 seconds
    • Ventilator modes: Airway pressure release ventilation (APRV) and high-frequency oscillatory ventilation (HFOV)
    • Prone positioning
  • Adverse events can occur with recruitment maneuvers and include hypotension, hypoxia, and pneumothorax (rare).

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Category: Critical Care

Title: Intensive BP Control in Spontaneous Intracranial Hemorrhage

Keywords: INTERACT 2, ATACH II, Intracranial Hemorrhage, Hypertensive Emergency, Hemodynamics (PubMed Search)

Posted: 2/24/2014 by John Greenwood, MD (Emailed: 2/25/2014) (Updated: 2/25/2014)
Click here to contact John Greenwood, MD

 

Intensive BP Control in Spontaneous Intracranial Hemorrhage

Managing the patient with hypertensive emergency in the setting of spontaneous intracerebral hemorrhage (ICH) is often a challenge.  Current guidelines from the American Stroke Association are to target an SBP of between 160 - 180 mm Hg with continuous or intermittent IV antihypertensives.  Continuous infusions are recommended for patients with an initial SBP > 200 mm Hg.
 

An emerging concept is that rapid and aggressive BP control (target SBP of 140) may reduce hematoma formation, secondary edema, & improve outcomes.
 

Recently published, the INTERACT 2 trial (n=2,829) compared intensive BP control (target SBP < 140 within 1 hour) to standard therapy (target SBP < 180) found:

  • No difference in mortality (11.9% vs 12%, respectively)
  • Improved functional status (secondary outcome) with intensive BP control
  • Intensive lowering of BP in patients with acute ICH appears safe 

Study flaws: Patients treated with multiple drugs - combinations of urapadil, labetalol, nicardipine, nitrates, hydralazine, and diuretics.  Management variability away from protocol seemed high. (Interesting editorial)
 

A Post-hoc analysis of the INTERACT 2 published just this month suggests that large fluctuations in SBP (>14 mmHg) during the first 24 hours may increase risk of death & major disability at 90 days.

 

Bottom Line:  INTERACT 2 was a large RCT but not a great study (keep on the look out for ATACH II).  However, in patients with spontaneous ICH, consider early initiation of an antihypertensive drip (preferably nicardipine) in the ED to reduce blood pressure fluctuations early with a target SBP of 140 mmHg.

 

Follow me on Twitter: @JohnGreenwoodMD

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  • The well-known effects of cocaine toxicity include seizures, cardiac ischemia, and rhabdomyolysis. Abdominal pain, however, is a lesser known side-effect and may occur secondary to ischemia, infarction or perforation of the gastrointestinal tract; such cases tend to occur in younger people without known risk factors for ischemia.
  • Ischemia may occur from the direct vasoconstrictive effects of cocaine, but may also occur from its pro-thrombotic effects on the mesenteric vessels; although any segment of the GI tract may be involved, the small bowel is most often affected.
  • Symptoms may vary from mild abdominal pain to bloody diarrhea. Physical exam may reveal peritoneal signs if perforation occurs.
  • CT scan of the abdomen may reveal the diagnosis although angiography may required for diagnosis or to guide revascularization.
  • Management may vary from conservative (i.e., bowel rest and antibiotics) to surgical exploration and bowel resection in selected cases.

 

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Category: Critical Care

Title: How to warm your frozen patient

Keywords: accidental hypothermia, rewarming, ecmo, artic sun (PubMed Search)

Posted: 2/11/2014 by Feras Khan, MD (Updated: 7/22/2024)
Click here to contact Feras Khan, MD

A 50yo man found dow in the snow was brought into our ER last week in cardiac arrest with a bladder temperature of 21° C. Let’s warm him up!

  • Passive external warming (good for mild hypothermia > 34° C):  remove all wet clothing, use warm blankets, hot chocolate.
  • Active external rewarming (Used for temp between 30-34° C): Radiant heat, electric blankets, Bair-Hugger. Disadvantages: “core temperature after drop” theory: drop in core temp because of peripheral vasodilatation. Therefore, focus on warming the chest and torso area.  May not occur with certain warming techniques.
  • Active core rewarming (<30 °C, above techniques and several other options):
  1. Heated humidified oxygen via mechanical ventilation at 42-46°
  2. IV normal saline warmed to 41-43° C
  3. Cardio-pulmonary bypass: 1-2° C increase every 5 minutes
  4. ECMO (best option in cardiac arrest): Up to 4-6° C/hr. VV or VA ECMO. Provides Cardio-pulmonary support. Can continue CPR while placing a cannula.
  5. CVVH: less costly, more available, 1-4°C/hr. Case reports only. 
  6. Artic Sun; external rewarming pads: used in hypothermia protocols. Easy to use. Case reports only.
  • Other methods (use if other methods are unavailable):
  1. Pleural irrigation: one chest tube in the mid-clavicular line w saline at 42° and another chest tube in the post-axillary line and connected to a pleurovac.
  2. Peritoneal lavage: 8 Fr catheter into the peritoneum using a standard paracentesis method. Use 40-45° C dialysate.
  3. Gastric, bladder, colonic irrigations

We were able to get ROSC with CPR and ACLS and then used Artic Sun to re-warm successfully.

Other tips/tricks:

  • Continue CPR while rewarming (This is debatable: monitor ECG for new rhythms)
  • How warm is “warm and dead”? Probably around 32°C
  • How fast to rewarm?  Would warm quickly in cardiac arrest and then 1-2° C/hr thereafter; (No good evidence here)
  • Arrhythmias corrected by rewarming (bradycardia etc); no need for pacing
  • Up to three defibrillations for V. fib/V. tach; hold if no benefit
  • Can give epinephrine per ACLS protocol but would be cautious with further dosing
  • Pressors: can use epinephrine drip cautiously for hypotension
  • Cisaturacurium for paralysis w/ sedation to prevent shivering
  • Rule out hypoglycemia, adrenal insufficiency, hypothyroidism, sepsis if patient does not rewarm as expected!
  • Avoid IJ lines or irritating the myocardium with a guidewire.
  • K>12 mmol /L: consider termination of CPR

Attachments

1402111256_nejm_hypothermia2012.pdf (581 Kb)



Category: Critical Care

Title: Mechanical Ventilation During ECMO

Keywords: VV-ECMO, mechanical ventilation, ultra-lung protective ventilation (PubMed Search)

Posted: 2/4/2014 by Mike Winters, MBA, MD
Click here to contact Mike Winters, MBA, MD

Mechanical Ventilation During ECMO

  • ECMO is a rapidly emerging therapy for critically ill patients with severe acute respiratory failure (VV-ECMO) and circulatory failure (VA-ECMO).
  • Mechanical ventilation (MV) settings may have important effects on patients receiving either VV- or VA-ECMO.
  • Though no large, randomized trials, consensus guidelines and expert opinion recommend the following initial settings for patients receiving VV-ECMO:
    • Tidal volume: < 4 ml/kg predicted body weight
    • Plateau pressure: < 25 cmH2O
    • PEEP: 10-15 cmH2O
    • FiO2: titrated to maintain sats > 85%
    • RR: 4 to 6 breaths per minute

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NSSTIs occur secondary to toxin-secreting bacteria; NSSTIs are surgical emergencies with a high-morbidity / mortality

Risk factors: immunocompromised host (DM, AIDS, etc.), intravenous drug use, malnourishment, peripheral vascular disease

Type I (polymicrobial; most common), Type II (monomicrobial; typically clostridia, streptococci, staph, or bacteroides), Type III (Vibrio vulnificus; seawater exposure)

Signs / Symptoms: pain out of proportion to exam (occasionally no pain at all), skin findings (blistering / bullae, gray-skin discoloration, or “Dishwater-like” discharge), or systemic toxicity (altered mental status, elevated lactate, etc.)

Diagnostic radiology

  • Xray (shows gas); low sensitivity; CT scan (gas / tissue stranding); sensitivity is also low
  • MRI can over-diagnose NSSTI and should not be used routinely
  • Bedside ultrasound may demonstrate fluid or gas collections in deeper tissues (see clip below)

Treatment is emergent surgical debridement with simultaneous hemodynamic resuscitation PLUS broad-spectrum antibiotics; consider clindamycin becuase it has anti-toxin activity

Adjunctive therapies include Intravenous intraglobulin (neutralizes toxins secreted by bacteria) and hyperbaric oxygen

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Category: Critical Care

Title: A-lines: A Significant Source of Preventable Blood Stream Infections

Keywords: arterial line, catheter related blood stream infections (PubMed Search)

Posted: 1/20/2014 by John Greenwood, MD (Emailed: 1/21/2014) (Updated: 1/21/2014)
Click here to contact John Greenwood, MD

 

Arterial Catheter-Related Blood Stream Infections

Whether arterial lines are a potential source of catheter-related blood stream infections (CRBSIs) is highly-debated; however, based on a recent systematic review they are an under recognized and significant source of CRBSIs.

  • IncidenceIn systematically cultured arterial catheters, the infection rate was 1.6 infections/1,000 catheter days which is similar to what has been reported for infections associated with short-term CVC's.
     
  • Location: Femoral a-lines are more likely than radial a-lines to be a source of a CRBSI. Femoral a-line CRBSIs occurred in 1.5% of all catheters (95% CI, 0.8–2.2%), which is higher than radial CRBSI, with a relative risk of infection 1.94 times greater than those placed at the radial site.
     
  • TechniqueOnly one study specifically evaluated the impact of full barrier precautions versus using sterile gloves only for peripheral a-lines, and it did not find any significant difference in BSI. No study has evaluated the impact of maximal barrier precautions for femoral, axillary, and brachial arterial catheters.
     
  • Dressing: The risk of infection was significantly decreased with the use of chlorhexidine-impregnated dressings (ex: BioPatch).

 

Bottom Line(s) 

  1. Arterial lines appear to be a significantly under recognized source of CRBSI's in critically-ill patients.  If you are deciding to place an a-line for invasive blood pressure monitoring, strongly consider the radial site and use a chlorhexidine sponge or dressing to try and minimize the risk of future BSI.
     
  2. There is a paucity of data regarding the utility of maximal barrier techniques when inserting peripheral arterial lines.  With arterial catheter infection rates approaching that of central venous catheters, we should probably be inserting a-lines with the same sterile technique.

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Determination of Brain Death

  • With the recent media spotlight on brain death (irreversible end of brain activity) due to a few recent cases, it would be helpful to review the definition.
  • Rule out alternative causes including hypothermia, drug-induced coma, metabolic abnormalities, or severe electrolyte disturbances.
  • A clear irreversible cause must be known based on history and diagnostic studies.

Clinical Examination

  • Patient should be unresponsive to verbal or noxious stimulation, with the exception of spinally mediated responses.
  • Absence of brainstem Reflexes
  1.             No pupillary response
  2.             Absent corneal reflex
  3.             Absent gag and cough reflex
  4.             Absent cervico-ocular reflex (Doll’s Eyes Maneuver)
  5.             Absent vestibulo-ocular reflex (Cold Calorics)
  • Apnea Testing  (disconnecting the ventilator and evaluating respiratory drive)

If apnea testing cannot be performed due to instability, hypoxia, or cardiac arrhythmias, then a confirmatory test should be performed (from highest to lowest sensitivity):

  •  Angiography (lack of intracranial flow)
  •   EEG
  •   Transcranial Doppler
  •   Technetium-99 brain scan
  •   Somatosensory evoked potentials

There is state to state variation on who can perform the test and how many separate examinations need to be performed before brain death can be legally declared.

For a great review on some of the pitfalls in making the diagnosis and difficulties with the examination, please see the attached article. 

 

Show References


Attachments

1401141409_pitfalls_in_brain_death,_wijdicks.pdf (93 Kb)



Category: Critical Care

Title: LVAD Pearls

Posted: 1/7/2014 by Mike Winters, MBA, MD (Updated: 7/22/2024)
Click here to contact Mike Winters, MBA, MD

Pearls for the Crashing LVAD Patient

  • Left ventricular assist devices (LVAD) are placed as a bridge to transplant, bridge to recovery, or as destination therapy.
  • As thousands of LVADs have been implanted, it is likely that a sick LVAD patient will show up in your ED or ICU.
  • In addition to pump thrombosis (UMEM pearl 12/31/13), two complications to also consider in the crashing LVAD patient include infection and arrhythmias.
  • Infection:
    • The driveline and pump pocket are the most common locations for device infection.
    • Most are caused by Staphylococcus and Enterococcus organisms.
    • For pump pocket and deeper wound infections be sure to also add coverage against Pseudomonas species. 
  • Arryhthmias:
    • The highest incidence is within the first month after implantation.
    • Consider a "suction event," where the inflow cannula contacts the ventricular septum.
    • Suction events can be caused by hypovolemia, small ventricular size, or RV failure and are treated with fluid resuscitation and decreasing the LVAD speed.

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