UMEM Educational Pearls - By Mike Winters

Drug-Induced Thrombocytopenia

  • Thrombocytopenia is common in critically ill patients and is associated with increased mortality.
  • Up to 25% of critically ill patients will develop thrombocytopenia as a result of a medication, termed drug-induced thrombocytopenia (DIT)
  • Antibiotcs are a common, yet infrequently recognized, cause of DIT.
  • Antibiotics reported to cause DIT include linezolid, vancomycin, trimethoprim/sulfamethoxazole, and the beta-lactams.
  • In fact, piperacillin/tazobactam has been associated with DIT more frequently than any other penicillin. 

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Category: Critical Care

Title: ICU Acquired Weakness

Posted: 7/19/2010 by Mike Winters, MD (Emailed: 7/20/2010) (Updated: 9/27/2022)
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ICU Acquired Weakness

  • ICU acquired weakness (ICU-aw) is a general term that refers to the weakness that develops in critically ill patients during the course of their illness - especially in patients with sepsis and those receiving mechanical ventilation.
  • ICU-aw is an very common complication of critical illness that can develop within hours and has been shown to increase the duration of mechanical ventilation and ICU/hospital LOS.  Observational studies have also reported an association with mortality.
  • Risk factors associated with ICU-aw include medications (neuromuscular blocking agents, corticosteroids), hyperglycemia and immobility.
  • For the critically ill ED patient, current recommendations suggest limiting the administration of neuromuscular blocking agents and corticosteroids, when possible.

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Drug-Drug Interactions in the Critically Ill

  • Critically Ill ED patients are at risk for drug-drug interactions (DDIs) due to altered organ function, polypharmacy, and altered drug kinetics.
  • DDIs involving the cytochrome isoenzyme CYP3A4 are of particular importance.
  • CYP3A4 inhibitors, such as macrolides and azoles (fluconazole, voriconazole), can cause serious DDIs when given concomitantly with meds that are a subtrate for CYP3A4 - midazolam, cyclosporine, tacrolimus, diltiazem, amiodarone.
  • Pay particular attention to your transplant patients, as administration of an azole can result in significant cyclosporine or tacrolimus toxicity.

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Asthma, Peak Pressures, and the Ventilator

  • In previous pearls, we have highlighted ventilator settings for the asthmatic, along with the differences between peak and plateau pressure measurements.
  • When ventilating the asthmatic, pay attention to the ventilator settings placed by your respiratory therapist.
  • In general, the respiratory therapist will set the ventilator to stop delivering tidal volumes when the peak pressure exceeds 40-60 cm H2O.
  • For asthmatics, this practice can result in very low tidal volumes.
  • Thus, peak pressure limits must be set higher.
  • As you know, high peak pressures have not been shown to be injurious, provided that the plateau pressure remains < 30 cm H2O

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Category: Critical Care

Title: Acidosis and Intubation

Posted: 6/29/2010 by Mike Winters, MD (Updated: 9/27/2022)
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Pre-existing acidosis and mechanical ventilation

  • Not surprisingly, many critically ill ED patients often develop a metabolic acidosis.
  • To compensate, patients hyperventilate, thereby producing a respiratory alkalosis.
  • When these patients require intubation and mechanical ventilation, be sure to provide the same level of respiratory compensation when setting the ventilator. 
  • Failing to provide a rate sufficient to compensate for the pre-intubation acidosis leads to a rapid drop in pH, bradycardia and eventually asystole.
  • In general, rates can be increased to about 30-35 breaths per minute, after which auto-PEEP becomes problematic.

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Category: Critical Care

Title: Hypotension and MV

Posted: 6/15/2010 by Mike Winters, MD (Updated: 9/27/2022)
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Hypotension after intubation and initiation of mechanical ventilation

  • Approximately 25-30% of patients develop hypotension after intubation and initiation of mechanical ventilation (MV).
  • Although the literature is not robust, risk factors for hypotension after initiation of MV include:
    • hypotension prior to intubation
    • tachycardia prior to intubation
    • obesity
    • high intrathoracic pressure (COPD)
    • excess catecholamine states (ETOH withdrawal, cocaine intoxication) with rapid relaxation during RSI
  • In addition to administering isotonic intravenous fluids (IVFs) while preparing for intubation, consider having a vasopressor medication, such as phenylephrine, available if IVFs alone prove insufficient at maintaining blood pressure.

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Platelet Transfusions in the Critically Ill

  • Recommendations for the transfusion of platelets in the critically ill patient is primarily extrapolated from the oncology literature; literature that is predominantly observational and expert opinion.
  • Nevertheless, indications for the transfusion of platelets in a critically ill ED patient include:
    • active bleeding with a plt count < 50 x 109/L
    • plt count < 10 x 109/L (high risk of spontaneous bleeding)
    • prior to an invasive procedure when the plt count is < 50 x 109/L
  • Importantly, the decision to transfuse platelets should also take into account the clinical setting (ie. a uremic patient with active bleeding)

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Postcardiac Arrest Syndrome: Controlled Reoxygenation

  • In previous pearls, Dr. Marcolini has highlighted the poscardiac arrest syndrome (PCAS), comprised of brain injury, myocardial dysfunction, systemic ischemia/reperfusion response, and persistent precipitating disease.
  • Not surprisingly, postcardiac arrest brain injury is a major cause of morbidity and mortality, accounting for > 60% of deaths in some studies.
  • In addition to therapeutic hypothermia, consider "controlled reoxygenation" in order to optimize neurologic outcome.
  • Animal data has demonstrated that too much oxygen may worsen neuronal damage during the initial resuscitation phase.
  • Take Home Points:
    • Use a minimum amount of FiO2 to maintain SpO2 of 94-96%
    • Avoid unnecessary arterial hyperoxia

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Category: Critical Care

Title: PRBCs in Neurocritical Care

Posted: 5/11/2010 by Mike Winters, MD (Updated: 9/27/2022)
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PRBC Transfusions in Neurocritical Care

  • Historically, neurocritical care textbooks have favored a more liberal PRBC transfusion strategy, as the brain is very sensitive to decreases in oxygen delivery.
  • Despite these recommendations, limited studies have failed to show a mortality benefit to PRBC transfusion in critically ill patients with neurologic illness.
  • Postulated reasons for the lack of morbidity or mortality benefit center around the injured brain's response to attempts to increase oxygen delivery through transfusion.
    • TBI: PET studies have shown an overall lower level of metabolic activity along with a lower oxygen extraction and loss of autoregulation
    • SAH: transfusion may increase the risk of vasospasm in SAH and worsen flow
  • Although the evidence is not overwhelming, current recommendations from SCCM-Eastern Society for the Surgery of Trauma recommend a restrictive PRBC transfusion threshold (Hgb < 7 gm/dL) even in neurocritical care patients.

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PRBC Transfusion Threshold for Patients with Cardiac Disease

  • As previously discussed, the PRBC transfusion threshold for the general population of critically ill patients is a Hgb < 7 gm/dL.
  • Traditional teaching has been to maintain a Hgb > 10 gm/dL in patients with a history of CAD.
  • This threshold stems from a 1950s cohort of Jehovah's Witness patients, and several observational studies, that demonstrated increased perioperative mortality in patients whose Hgb was < 10 gm/dL.
  • Recent studies, however, have found that patients with a history of CAD tolerate lower Hgb levels without increases in morbidity or mortality.  In fact, current cardiovascular surgery guidelines favor a conservative Hgb threshold (7 gm/dL) for patients with CAD.
  • Importantly, the Hgb threshold of < 7 gm/dL for PRBC transfusion applies to patients with simply a history of CAD and not to patients with evidence of an acute coronary syndrome (STEMI, NSTEMI, unstable angina).  Guidelines continue to recommend a Hgb > 10 gm/dL for patients with ACS.

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Category: Critical Care

Title: Type B Lactic Acidosis

Posted: 4/13/2010 by Mike Winters, MD (Updated: 9/27/2022)
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Type B Lactic Acidosis

  • In the critically ill, patients may often have elevated lactate levels without ongoing tissue hypoperfusion.
  • In these patients it is important to consider the causes of what is referred to as "Type B Lactic Acidosis".
  • Pertinent to critically ill ED patients, consider the following:
    • Type B1 - related to underlying disease
      • renal faiilure
      • hepatic failure
      • malignancy
      • HIV
    • Type B2 - effects of drugs/toxins
      • acetaminophen
      • alcohols
      • beta-adrenergic agents: epinephrine
      • cocaine, methamphetamine
      • propofol
      • salicylates
      • valproic acid
      • metformin
    • Type B3 - inborn errors of metabolism

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Ventilator Pearls for H1N1 Influenza Virus

  • As the spring/summer travel season begins, it is predicted that we will see additional cases of H1N1
  • The most common presentation requiring ICU admission to date has been a viral pneumonitis
  • As highlighted in previous pearls, the hallmark of disease has been refractory hypoxemia requiring mechanical ventilation in about 85% of patients.
  • Current recommendations for H1N1 respiratory failure:
    • Consider early intubation
    • Noninvasive ventilation has been unsuccessful in most and should generally be avoided
    • Low tidal volume settings (6 ml/kg) with PEEP based on FiO2 to maintain SpO2 > 88% and plateau pressure < 35 cm H2O
    • Although there is no proven mortality benefit to rescue therapies such as recruitment maneuvers, neuromuscular blockade, and prone ventilation, these can be considered in discussion with your intensivist.

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Category: Critical Care

Title: Warfarin and ICH

Posted: 3/16/2010 by Mike Winters, MD (Updated: 9/27/2022)
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Warfarin and ICH

  • Warfarin causes approximately 10-15% of all intracerebral hemorrhages (ICH)
  • Many warfarin-related ICHs occur with INRs in the therapeutic range
  • Patients with warfarin-related ICH have higher mortality and typically suffer worse neurologic outcome
  • The primary pitfall in treating patients with warfarin-related ICH is the failure to rapidly normalize the INR
  • Do not delay treatment while awaiting the results of coagulation labs
  • Patients should receive IV vitamin K via slow infusion and FFP
  • Prothrombin Complex Concentrate (PCC) is gaining popularity but much of the supporting literature uses agents not available in the US
  • Similarly, there is no significant evidence that recombinant factor VIIa improves outcomes in patients with warfarin-related ICH

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Category: Critical Care

Title: Vent Strategies for TBI

Posted: 3/2/2010 by Mike Winters, MD (Updated: 9/27/2022)
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Ventilating the Patient with Traumatic Brain Injury

  • Many patients with acute TBI will require intubation and mechanical ventilation for a variety of reasons.
  • Ventilating the patient with TBI becomes a balancing act between maintaining adequate cerebral perfusion and minimizing lung injury.
  • Some pearls to consider:
    • Avoid hypoxia: although guidelines recommend a PaO2 > 60 mm Hg, most suggest a higher PaO2 (> 80 mm Hg) be initially targeted.
    • Avoid hypercapnia:  many patients will develop hypercapnia when ventilated using the low tidal volume strategy (6 ml/kg) of the ARDSnet trial; titrate TVs to maintain a PaCO2 between 32-35 mm Hg.
    • PEEP: the application of PEEP remains controversial in patients with TBI given the theoretical risk of increasing ICP through reductions in venous return; if PEEP is applied pay close attention to the cerebral perfusion pressure to ensure it remains > 60 mm Hg.

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The Rapid Ultrasound in Shock (RUSH) Exam

  • Evaluating the ED patient with undifferentiated shock can be challenging.
  • Ultrasound can be an invaluable tool in helping to differentiate between hypvolemic, cardiogenic and obstructive shock.
  • The RUSH exam essentially focuses on the evaluation of the "pump", the "tank" and the "pipes".
  • The pump: exclude pericardial effusion, global estimate of LV EF, and determine if RV strain is present.
  • The tank: evaluate the IVC/jugular veins for volume status, look for fluid in the thorax/peritoneum, and exclude pulmonary edema or pneumothorax.
  • The pipes: look for a ruptured AAA or aortic dissection and DVT.

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Category: Critical Care

Title: Defining AKI

Posted: 1/19/2010 by Mike Winters, MD (Updated: 9/27/2022)
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Defining Acute Kidney Injury (AKI)

  • In the pearl from 1/5/10, I highlighted the association of AKI with increased morbidity and mortality in the critically ill along with the avoidance of nephrotoxic medications.
  • Currently, two sets of criteria (RIFLE and AKIN) can be used to identify patients with AKI
  • According to AKIN, the current diagnostic criteria for AKI is:
    • an absolute increase in serum creatinine > 0.3 mg/dL OR
    • a > 50% increase in serum creatinine from patient baseline OR
    • urine output < 0.5 ml/kg/hr for > 6 hours
  • For the critically ill ED patient, the most common causes of AKI include sepsis, hypovolemia, medications, trauma, rhabdomyolysis, obstruction and abdominal compartment syndrome

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Category: Critical Care

Title: AKI and the Critically Ill

Posted: 1/5/2010 by Mike Winters, MD (Updated: 9/27/2022)
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AKI and the Critically Ill

  • Acute kidney injury (AKI) is an abrupt reduction in kidney function causing disturbances in electrolytes, fluids, and acid-base balance.
  • AKI occurs in up to 67% of critically ill patients and is associated with a substantial increase in morbidity and mortality.
  • AKI in the critically ill is often multifactorial and most commonly due to sepsis, hypovolemia, medications, and hemodynamic instability.
  • Medications account for up to 20% of AKI in the critically ill.
  • Common medications that cause, or exacerbate AKI, in the critically ill include:
    • NSAIDS
    • Antibiotics (aminoglycosides, amphotericin, acyclovir)
    • ACE-inhibitors
    • Radiocontrast dye
  • Take Home Point:  AKI is common in our critically ill ED patients and, whenever possible, avoid nephrotoxic medications that can result in additional injury.

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Appropriate Antimicrobial Therapy for Sepsis

  • In previous pearls, we have discussed the importance of early antimicrobial administration for patients with sepsis.
  • In patients with septic shock, current guidelines recommend empiric antimicrobial therapy be initiated within 1 hour.
  • Equally as important as early administration is the selection of appropriate antimicrobial therapy (i.e. choosing an antibiotic that is effective against the presumed or identified pathogen).
  • In one of the most recent studies, investigators found a 5-fold reduction in survival (52% vs. 10.3%) between patients who received appropriate antibiotics compared to those who received antibiotics that were ineffective against the identified pathogen.
  • In fact, choosing the right antibiotic is one of the strongest factors associated with patient outcome in sepsis.
  • When selecting empiric antimicrobial therapy for patients with septic shock consider patient history, co-morbidities, the clinical site of infection, and local resistance data.

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Category: Critical Care

Title: Shock Index

Posted: 12/8/2009 by Mike Winters, MD (Updated: 9/27/2022)
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Early Recognition of Shock

  • Early recognition, and thus early treatment, of shock is crucial in reducing morbidity and mortality in the critically ill ED patient.
  • Traditionally, the diagnosis of shock has been based on vital sign abnormalities such as tachycardia, tachypnea, oliguria, etc.
  • Vital sign abnormalities have been shown to be insensitive markers of shock in the critically ill.
  • The Shock Index, although clearly not 100% sensitive, can assist in the detection of shock compared to heart rate and blood pressure alone.
  • Shock Index is simply heart rate divided by systolic blood pressure.
  • Values greater than 0.9 are abnormal and suggest markedly impaired cardiac output.

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Category: Infectious Disease

Title: Spinal Epidural Abscess

Posted: 11/24/2009 by Mike Winters, MD (Updated: 9/27/2022)
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Spinal Epidural Abscess Pitfalls

  • The classic triad of back pain, fever, and neurologic deficits are found in < 15% of patients at the time of presentation
  • Up to 75% will be afebrile
  • Up to 67% will have a normal initial neurologic exam
  • < 40% have a WBC greater than 12,000 cells/mm3
  • < 33% will have an abnormality on plain film in the first 7-10 days

Take Home Point: In the patient with risk factors for spinal epidural abscess (IVDU, DM, indwelling catheters, etc) do not exclude the diagnosis based upon the absence of a fever, a normal WBC count, and a normal neurologic exam.