UMEM Educational Pearls - By Mike Winters

Title: Noninvasive Ventilation Pearls

Category: Critical Care

Keywords: noninvasive ventilation (PubMed Search)

Posted: 7/15/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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 Noninvasive Ventilation Pearls

  • Multiple studies support the use of noninvasive positive pressure ventilation (NPPV) in acute exacerbations of COPD, acute cardiogenic pulmonary edema, and immunocompromised patients (organ transplant) with hypoxic respiratory failure.
  • The timing of NPPV initiation is important.  NPPV should be started as soon as possible, as delays increase the likelihood of intubation
  • The best predictor of success is a favorable response to NPPV within the first 1 to 2 hours
    • reduction in respiratory rate
    • improvement in pH
    • improved oxygenation
    • reduction in PaCO2
  • Also crucial to NPPV success is a well fitting interface (mask)
  • Although patients report greater comfort with nasal masks, they also permit more air leakage through the mouth and have been associated with a higher rate of initial intolerance in the acute setting.
  • For acute applications of NPPV in the ED, a full face mask is preferred 

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Title: Redefining Hypotension

Category: Critical Care

Keywords: hypotension, trauma, elderly (PubMed Search)

Posted: 7/7/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Hypotension begins at 110 mmHg?

  • Many of us use the historical SBP cut-off point of 90 mmHg or less to identify hypotension and shock
  • Importantly, there is no data to support this arbitrary value
  • Particularly in older patients, hypotension, hypoperfusion, and increased mortality may begin sooner than previously realized
  • In this study of over 80,000 patients from the National Trauma Data Bank, a SBP < 110 mmHg was found to be more clinically relevant for identifying hypotension and hypoperfusion
  • Take Home Point: strongly consider raising your threshold for identifying hypotension and initiating resuscitation, especially in the older trauma patient.

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Title: Etomidate and adrenal suppression

Category: Critical Care Literature Update

Keywords: etomidate, adrenal insufficiency (PubMed Search)

Posted: 7/7/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Recent Articles from the Critical Care Literature

Duration of adrenal insufficiency following a single dose of etomidate in critically ill patients

Vinclair M, Broux C, Faure P, Brun J, Genty C, et al. Intensive Care Med 2008;34:714-9.
            Etomidate has become a favored first-line induction agent for intubation in the emergency department.  Given its excellent hemodynamic tolerance, etomidate is especially useful in hemodynamically unstable patients. A known side effect of etomidate is adrenal suppression, due to inhibition of 11β-hydroxylase, the enzyme that converts 11β-deoxycortisol into cortisol. As a result, recent literature has raised concerns that etomidate may worsen patient outcomes in those with relative adrenal insufficiency, namely those with septic shock.
            The current study is a prospective, observational study conducted in France from October 2005 to January 2006. The purpose of the study was to assess the duration of adrenal suppression following a single dose of etomidate, given either in the field or in the emergency department for RSI. Importantly, patients with septic shock, or those with preexisting adrenal insufficiency, were excluded from this study. To diagnose adrenal insufficiency, the investigators measured total cortisol and 11β-deoxycortisol following a high-dose cosyntropin stimulation test (250 mcg). Values were obtained at 12, 24, 48, and 72 hours following etomidate administration. An accumulation of 11β-deoxycortisol with a lack of cortisol rise was used to establish etomidate-related adrenal insufficiency.
            A total of 40 patients were included in this study. The majority of patients required intubation as a result of either trauma or subarachnoid hemorrhage. At hour 12, 80% of patients fulfilled the investigators definition of etomidate-related adrenal insufficiency, whereas by hour 48, only 9% met criteria. In addition, at hour 24, patients with etomidate-related adrenal suppression required larger doses of norepinephrine that those without adrenal inhibition. From their data, the authors conclude that a significant proportion of patients without septic shock have adrenal suppression for at least 12 hours following a single dose of etomidate. This effect, however, appeared reversible in that most patients recovered adrenal function by hour 48. Finally, the authors recommend that systemic steroid supplementation be considered during the first 48 hours in hemodynamically unstable patients who have received etomidate for intubation.
            There are a number of limitations with this study. The most important limitation is, perhaps, the authors’ definition of etomidate-related adrenal insufficiency. Diagnosing adrenal insufficiency in critically ill patients remains controversial. The cosyntropin test (high- or low-dose) has many recognized limitations. In addition, measurement of 11β-deoxycortisol is difficult because reference values for critically ill patients are rare. The authors also chose to measure total serum cortisol, rather than the more biologically active free serum cortisol. Lastly, data for all 40 patients at 72 hours was not complete.
            Take Home Points: This small, observational study found a high incidence of adrenal suppression for at least the first 12 hours in unstable patients receiving etomidate for intubation. Importantly, this study excluded patients with sepsis or septic shock. Given the limited number of patients and the difficulty in defining adrenal insufficiency in the critically ill, this study provides some interesting results and is hypothesis-generating at best. Their recommendation for systemic steroid supplementation during the first 48 hours following etomidate administration in unstable patients cannot be supported by this study.


Title: recombinant Factor VIIa for ICH

Category: Critical Care Literature Update

Keywords: intracerebral hemorrhage, recombinant factor VIIa (PubMed Search)

Posted: 7/6/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Recent Articles from the Critical Care Literature

Efficacy and Safety of Recombinant Activated Factor VII for Acute Intracerebral Hemorrhage.

Mayer SA, Brun NC, Begtrup MSc, Broderick J, Davis S, et al. NEJM 2008;358:2127-37.
            Intracerebral hemorrhage (ICH) accounts for approximately 10% to 15% of all strokes, yet has the highest morbidity and mortality, with up to 40% of patients dying within 30 days. Aside from age, size, location, intraventricular extension, and GCS, hematoma expansion is an independent determinant of morbidity and mortality. Hematoma expansion is reported to occur in up to 70% of patients within the first several hours of the ICH. Recent research has focused on therapies to limit hematoma expansion. One such therapy is recombinant human activated Factor VII (rFVIIa). Excitement regarding this expensive drug came from a single phase 2 trial (Mayer SA, et al. NEJM 2005:352:777-85.) that demonstrated rFVIIa significantly reduced hematoma expansion and improved patient mortality.
            The FAST trial (Factor Seven for Acute Hemorrhagic Stroke), was a manufacture sponsored, phase 3 trial performed by the same investigators to confirm the findings of their previous phase 2 study. The FAST trial was a multi-center, randomized, double-blind, placebo-controlled trial conducted at 122 sites in 22 countries. Patients had to be at least 18 years of age with a spontaneous ICH documented by CT within 3 hours of symptom onset. Important exclusion criteria included GCS < 5 at presentation, secondary ICH (trauma, AVM), current anticoagulant therapy, thrombocytopenia, DIC, previous disability from CVA, or a thromboembolic event < 30 days prior to symptom onset. The primary end-point was disability or death defined by a modified Rankin score of 5 or 6 at day 90. The modified Rankin score evaluates global disability and handicap and ranges from 0 to 6. A score of 5 indicates a patient who is bed-bound and incontinent, whereas a score of 6 indicates death.
            Of 8,886 patients screened, 821 underwent randomization and received placebo, 20 mcg/kg of rFVIIa, or 80 mcg/kg of rFVIIa. Treatment had to start within 1 hour of the baseline CT and no more than 4 hours after the onset of symptoms. Patients then underwent a repeat CT at 24 hours and 72 hours to evaluate for hematoma expansion. Of note, the majority of the patients in this study were Caucasian males, older than 65 year of age who had deep gray matter ICHs. 
            As reported by the trial investigators, rFVIIa did reduce hematoma expansion at 24 hours compared to placebo. In the placebo arm, 26% of patients had hematoma growth, whereas only 11% of patients who received 80 mcg/kg of rFVIIa had hematoma expansion. In addition, the investigators report that the reduction in hematoma growth was even greater in those treated in less than 2 hours from onset of symptoms. However, when you look at the data for 72 hours, there was no significant difference in total hematoma volume or edema volume. More importantly, mortality at 90 days did not differ between placebo and the treatment groups. In fact, a higher percentage of patients who received 80 mcg/kg of rFVIIa had a worse outcome than compared with placebo. Furthermore, there was an absolute increase of 5% in the frequency of arterial thromboembolic serious events (MI, ischemia CVA) in the group receiving 80 mcg/kg of rFVIIa.
            Take Home Point: This phase 3 trial failed to demonstrate improved 90 day mortality in patients with spontaneous ICH who received rFVIIa. Although hematoma expansion was reduced at 24 hours in the rFVIIa groups, total lesion volume and edema volume at 72 hours remained unchanged. Although rFVIIa has been used in a variety of clinical settings, the results of this study indicate that it does improve mortality in patients with spontaneous ICH. Given the expense of the drug and lack of benefit, this should not be a drug we are using in the ED to treat patients with spontaneous ICH.


Title: Diabetes and Osteomyelitis

Category: Infectious Disease

Keywords: diabetes, osteomyelitis, temperature, white blood cell count (PubMed Search)

Posted: 7/1/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Does this Patient with Diabetes have Osteomyelitis?

  • Diagnosis of lower extremity osteomyelitis in the diabetic patient remains challenging
  • Bone biopsy with culture remains the gold standard for diagnosis but is not always obtainable
  • What clinical features, therefore, raise the likelihood of osteomyelitis?
  • In this review, an ulcer size > 2 cm2 (LR 7.2), ability to probe to bone using a sterile stainless steel probe (LR 6.4), and an ESR > 70 mm/h were found to be useful in predicting the presence of osteomyelitis
  • Clinical features NOT found to be useful included fever (sensitivity 19%), presence of erythema, swelling, or purulence (LR 1), elevated white blood cell count (sensitvity 14%-54%), and superficial swab culture
  • A note about radiographic studies:
    • bony changes on plain films may take up to 2 weeks to develop
    • plain films alone are only marginally useful if positive (LR 2.3)
    • MRI is more accurate than bone scan or plain films
    • If you are going to order a radiographic study, your best bet is the MRI

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Title: Passive Leg Raising

Category: Critical Care

Keywords: passive leg raising, fluid responsiveness (PubMed Search)

Posted: 6/17/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Passive Leg Raising (PLR)

  • We have discussed that static measures of volume (CVP, PA wedge pressures) are not reliable markers of fluid responsiveness
  • PLR has recently gained interest as a simple and transient way to assess fluid responsiveness in the critically ill
  • Patients are placed in the horizontal position (not Trendelenburg) and the legs are raised to 45 degrees
  • A hemodynamic response should be seen in 30 - 90 seconds
  • Patients who have improvement in hemodynamics with PLR are said to be fluid responsive (i.e on the ascending portion of their Starling Curve) and require additional volume resuscitation

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Title: Acinetobacter

Category: Critical Care

Keywords: acinetobacter, polymixin, ventilator-associated pneumonia, bacteremia (PubMed Search)

Posted: 6/3/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Acinetobacter in the Critically Ill

  • As all of us know, there has been an alarming increase in the incidence of acinetobacter infections
  • At present, infections mostly occur in ICU/critically ill patients
  • Important risk factors for colonization and infection include mechanical ventilation, recent surgery, tracheostomy, residents of long-term care facilities, central venous catheterization, and enteral feedings
  • The most frequent clinical manifestations are ventilator associated pneumonia and bacteremia
  • Susceptible strains can be treated with a broad-spectrum cephalosporin, carbapenem, or B-lactam-B-lactamase used alone or in combination with an aminoglycoside
  • For resistant strains, the most active agent in vitro are the polymyxins
  • The most common adverse effect of the polymyxins is nephrotoxicity (up to 36%)
  • Tigecycline has been used but resistance rates are rapidly increasing

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Title: Fluids and Acute Liver Failure

Category: Critical Care

Keywords: jlactated Ringer's solution, dextrose, cerebral edema (PubMed Search)

Posted: 5/27/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Fluids in Acute Liver Failure

  • Acute liver failure is often complicated by intravascular volume depletion - insensible losses, vomiting, poor oral intake
  • Early and adequate fluid resuscitation is mandatory
  • AVOID lactated Ringer's solution - exogenous lactate load is poorly tolerated by lack of hepatic function
  • AVOID dextrose containing water solutions - will lead to hyponatremia and increase the risk of cerebral edema

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Title: COPD and mechanical ventilation

Category: Critical Care

Keywords: bicarbonate, pH, COPD, mechanical ventilation (PubMed Search)

Posted: 5/20/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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COPD and mechanical ventilation

  • In some studies, the failure rate of non-invasive positive pressure ventilation (CPAP, BiPAP) in acute exacerbations of COPD has been as high as 50%
  • When setting the ventilator in patients with COPD, keep in mind that the majority have chronic ventilatory failure with a chronic compensatory respiratory acidosis
  • Pearl: Look at the serum bicarbonate level obtained from a recent period of stability
  • A recent serum bicarbonate level can provide an indirect indication of the patient's baseline PaCO2 if you have no prior ABGs
  • Rather than target a PaCO2 of 40 mm Hg, manipulate the ventilator to target the patient's baseline serum bicarbonate or a pH of 7.35 - 7.38.

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Title: PEEP in Acute Lung Injury

Category: Critical Care

Keywords: PEEP, acute lung injury, acute respiratory distress syndrome (PubMed Search)

Posted: 5/13/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Acute Lung Injury (ALI) / Acute Respiratory Distress Syndrome (ARDS)

  • ALI and ARDS are defined as:
    • bilateral pulmonary infiltrates on CXR
    • pulmonary capillary wedge pressure < 18 mm Hg (no heart failure)
    • PaO2 / FiO2 < 300 = ALI
    • PaO2 / FiO2 < 200 = ARDS
  • The current management for patients with ALI or ARDS is low tidal volume ventilation and a conservative fluid management strategy
  • Two recent trials (EXPRESS and LOVS) evaluated different applications of PEEP in patients with ALI/ARDS
  • Both studies evaluated lower levels of PEEP (5-10) vs. higher levels of PEEP titrated to plateau pressure
  • Bottom line: different PEEP strategies did not influence survival, although higher levels did result in improved oxygenation.


Title: Propofol Infusion Syndrome

Category: Critical Care

Keywords: propofol (PubMed Search)

Posted: 5/7/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Propofol Infusion Syndrome

  • Many of us are now using propofol for sedation in our critically ill patients
  • Although a great drug, it is important to be aware of "propofol infusion syndrome" (PIS)
  • Risk factors for PIS include young age, severe CNS or pulmonary illness, and exogenous catecholamine administration
  • Clinical features include: unexplained metabolic acidosis, rhabdomyolysis, hyperlipidemia, hepatomegaly, and cardiovascular instability
  • Pearl: It is reported that the development of coved ST elevations in V1-V3 (similar to Brugada syndrome) may be the first sign of cardiac instability with PIS

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Title: Intra-aortic balloon pump counterpulsation

Category: Critical Care

Keywords: intra-aortic balloon pump counterpulsation, cardiogenic shock (PubMed Search)

Posted: 4/29/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Intra-aortic balloon pump counterpulsation

  • It is possible that at some point in your career you may need to place an intra-aortic balloon pump (IABP) to temporarily stabilize a patient wth cardiogenic shock
  • Optimal performance of the IABP is dependent upon proper positioning in the thoracic aorta
  • Traditional teaching has been to insert the IABP via the femoral artery and advance to the level of the aortic knob (via CXR)
  • A recent study suggests that using the aortic knob to position the IABP may result in occlusion of the left subclavian artery in a substantial portion of patients (16% in the study)
  • Placing the IABP 2 cm above the carina may be a more reliable landmark that using the aortic knob

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Title: Bedside glucose

Category: Critical Care

Keywords: glucose, critically ill (PubMed Search)

Posted: 4/22/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Bedside Glucometry in the Critically Ill

  • Hyperglycemia is common in critically ill patients
  • Depending on the underlying condition (e.g. DKA), you may be instituting an insulin drip and following frequent fingersticks in the ED
  • A recent study indicates that bedside glucose values may not accurately reflect serum values in approximately 15% of critically ill patients
  • This is more likely to occur in patients with poor peripheral perfusion
  • Take Home Point: Interpret bedside glucose readings with caution especially in hypotensive critically ill patients

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Title: Vasopressing for sepsis

Category: Critical Care

Keywords: vasopressin, septic shock (PubMed Search)

Posted: 4/15/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Vasopressin for Sepsis

  • The VASST trial was recently published in NEJM comparing vasopressin vs. norepinephrine for septic shock
  • Unfortunately, there are some issues with the study which I will clarify/expand upon in the next Critical Care Literature Update
  • There was a trend towards improved mortality in the vasopressin group receiving low doses of norepinephrine (5 - 14 mcg/min)
  • Take Home Point: If you are thinking about adding vasopressin to norepinephrine in patients wtih refractory septic shock, do it early.  In other words, add vasopressin when you find yourself titrating norepinephrine doses to 6, 7, 8 mcg/min


Title: ACTH Stimulation Test

Category: Critical Care

Keywords: ACTH stimulation test, adrenal insufficency, corticosteroids (PubMed Search)

Posted: 4/8/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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ACTH Stimulation Test

  • With the recent publication of the CORTICUS study (along with others), it is becoming clear that the ACTH stimulation test is not reliable in identifying patients with adrenal insufficiency
  • In fact, the test is no longer recommended in the evaluation of patients with severe sepsis/septic shock
  • Furthermore, if you decide to give steroids to the patient with severe sepsis/septic shock, there is no need to use dexamethasone for fear of "disrupting the ACTH stim test" (hydrocortisone is the preferred agent)


Title: Dialysis disequilibrium syndrome

Category: Critical Care

Keywords: dialysis disequilibrium syndrome, mannitol, cerebral edema (PubMed Search)

Posted: 4/1/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Dialysis Disequilibrium Syndrome (DDS)

  • Although typically seen in ESRD patients who are being initiated on hemodialysis, DDS can be seen in the critically ill
  • Critically ill patients at risk for DDS include recent CVA, head trauma, subdural hematoma, hyponatremia,hypertensive emergency, and hepatic encephalopathy
  • Mild cases are characterized by restlessness, nausea, vomiting, headache, disorientation, and tremors
  • More severe symptoms include seizures and coma
  • The exact pathogenesis is debated but centers around acute cerebral edema
  • Treatment of DDS primarily centers around manipulation of hemodialysis
  • For the EP: patients with DDS presenting with seizures can be treated by rapidly increasing plasma osmolality with either hypertonic saline or mannitol (12.5 gms) 


Title: Guidewire length

Category: Critical Care

Keywords: central venous catheter, guidewire (PubMed Search)

Posted: 3/25/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Guidewire length for central venous catheterization

  • 18 cm should be considered the upper limit of guidewire insertion during internal jugular or subclavian central venous catheterization (16cm for right IJ)
  • There is the Peres Nomogram for determining guidewire length, which is based on patient height
  • However, height is less reliable in predicting safe guidewire length


Title: "K-Phos"

Category: Critical Care

Keywords: phosphate, hypotension, hypomagnesemia (PubMed Search)

Posted: 3/18/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Potassium Phosphate ("K-phos")

Over the weekend, I had a patient with Dr. Scott that had a phosphate of 0.8 mmol/L.  Phosphate < 1.0 mmol/L is an indication for IV repletion.  IV repletion involves giving potassium phosphate.  An important clinical question, therefore, is how much potassium does the patient actually get?

  • 1 mmol of IV phosphate delivers 1.46 mEq of potassium
  • Recommended infusion rate is 5 mmol/hr
  • Rapid infusion may lead to severe hypocalcemia, hypotension, acute renal failure, hypomagnesemia, and hypernatremia


Title: Coagulopathy and Trauma

Category: Critical Care

Keywords: fresh frozen plasma, coagulopathy, PRBC (PubMed Search)

Posted: 3/11/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Coagulopathy and Trauma

  • When resuscitating a trauma patient recall that the "lethal triad" consists of acidosis, hypothermia, and coagulopathy
  • Coagulopathy is induced by the combination of direct loss of clotting factors, consumption in clot formation, dilutional due to crystalloid administration, acidosis, and hypothermia
  • When giving PRBCs in trauma resuscitation, don't forget to give FFP
  • The ratio to remember is 1U of FFP for every 2U PRBCs


Title: Aspiration pneumonitis

Category: Critical Care

Keywords: aspiration pneumonitis (PubMed Search)

Posted: 3/4/2008 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Aspiration Pneumonitis

  • Aspiration pneumonitis is an acute lung injury resulting from the aspiration of gastric contents
  • It is an inflammatory condition rather than infectious
  • Despite the inflammation, corticosteroids have been shown to have no effect on mortality
  • Aspiration pneumonitis is self limited
  • Antibiotics are generally held for 24 to 48 hours
  • When to consider empiric broad spectrum antibiotics in the ED:  Gastric contents are sterile in most patients.  Patients who may have colonization/contamination of gastric contents are more likely to progress from pneumonitis to pneumonia.  Consider empiric antibiotics for aspiration pneumonitis in the patient with SBO, gastroparesis, those receiving enteral feeds through a G- or J-tube, and those on chronic PPI's/antacids.