UMEM Educational Pearls - By Mike Winters

Category: Critical Care

Title: Antibiotic Timing

Posted: 12/15/2010 by Mike Winters, MBA, MD (Updated: 8/14/2024)
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The Importance of Antibiotic Timing for Sepsis and Septic Shock

  • Septic shock is perhaps the most common critical illness that emergency physicians manage.
  • In several studies, delays in initiating antibiotics for patients with septic shock were the strongest predictor of mortality.
  • Broad spectrum antibiotics should be administered ASAP (preferably within 60 minutes) to patients with septic shock. 
  • Selection of antibiotics should be based on the presumed source, the antibiogram at your institution, and the patient's risk factors for resistant organisms.
     

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Beware Trendelenburg Positioning in the Critically Ill Obese Patient

  • When inserting a central venous catheter (CVC) into the internal jugular or subclavian vein, clinicians often place patients in the Trendelenburg position to increase the size of the vein.
  • When possible, avoid Trendelenburg position for CVC placement in the morbidly obese patient.
  • These patients can quickly deteriorate in this position due to reduced lung volumes, increased right heart pressures, decreased cardiopulmonary reserve, and the effects in intra-abdominal pressure.

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Positioning for Ventilated, Critically Ill Obese Patients

  • Up to one-quarter of patients in the ICU are obese, as defined by a BMI > 35 kg/m2
  • Obesity can significantly alter pulmonary physiology causing
    • reduced lung volumes
    • decreased compliance
    • abnormal ventilation to perfusion relationships
    • respiratory muscle inefficiency
  • For intubated obese patients, body position can affect ventilatory management
  • In the supine position, obese patients can have collapse of lung segments along with increased impedance of the diaphragm
  • Elevating the head of the bed to 30-45 degrees in intubated obese patients has been shown to improve tidal volumes and lower respiratory rates.

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Ventilation Pearls in the Post-Cardiac Arrest Patient

  • Some ventilation pearls from the recently released 2010 AHA guidelines include:
    • Set the tidal volume to 6-8 ml/kg ideal body weight
    • Titrate minute ventilation to achieve a PaCO2 between 40-45 mm Hg or PETCO2 between 35-40 mm Hg
    • Reduce the FiO2 to maintain SpO2 > 94%

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Ketamine for RSI in Hemodynamically Unstable ED Patients

  • Recall that ketamine acts as a sympathomimetic resulting in increases in heart rate, blood pressure, and ultimately cardiac output.
  • Because of its rapid transport across the blood-brain barrier, its sympathomimetic effects, and lack of significant adverse effects, ketamine is recommended by many organizations as a first line agent for RSI in unstable patients.
  • Important contraindications to ketamine include an acute coronary syndrome, aortic dissection, and acute heart failure.
  • Take Home Point: Consider using ketamine the next time you need to intubate a hypotensive, critically ill ED patient.

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Respiratory Distress in the Ventilated ED Patient

  • In the ventilated patient with respiratory distress, evaluation of peak and plateau pressures can help to identify the cause.
  • Isolated increases in peak pressure suggest increased resistance to airflow and should prompt consideration of the following:
    • kinked or twisted ET tube
    • patient biting ET tube
    • obstructed ET tube
    • bronchospasm
    • lower airway obstruction
  • Increases in plateau pressure suggest decreased pulmonary compliance and should prompt consideration of the following:
    • unilateral intubation
    • pneumothorax
    • pulmonary edema
    • worsening pneumonia
    • abdominal HTN/compartment syndrome

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Life-threatening Bleeding in Hemophilia A Patients

  • Although an infrequent occurrence, patients with Hemophilia A can present with life-threatening hemorrhage (e.g. ICH).
  • Recall that normal clotting factor levels range from 50-150 IU/dL - reported by the lab as 50-150%.
  • Life-threatening bleeding requires Factor VIII levels between 80-100%.  In general, each unit of FVIII/kg raises plasma levels by 2%.
  • Recombinant Factor VIII products are preferred over plasma derived concentrates or blood products and are dosed as:
    • FVIII - 50 IU/kg loading dose followed by infusion of 3 IU/kg/hr
  • In the event you don't have access to recombinant or plasma derived FVIII concentrates, cryoprecipitate (contains FVIII) can be used.

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Pulmonary Contusion and Ventilator Management

  • Pulmonary contusion is the most common injury in blunt thoracic trauma.
  • Patients with pulmonary contusion often present with hypoxia, hypercarbia and increased work of breathing.
  • Importantly, patients with pulmonary contusion have a low cardiopulmonary reserve.  Maintain a low threshold for initiating mechanical ventilation is these patients.
  • When starting mechanical ventilation, think about the following:
    • Patients are at high risk for developing ARDS
    • Most centers use a low tidal volume ventilatory strategy
    • Higher levels of PEEP may be necessary to recruit collapsed alveoli
    • High frequency oscillatory ventilation (HFOV) and airway pressure release ventilation (APRV) are modes of ventilation that are gaining in popularity for ventilating patients with pulmonary contusions.

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Hemostatic Therapy for ICH - Updated Guidelines

  • The AHA/ASA just published updated guidelines for the diagnosis and treatment of acute spontaneous intracerebral hemorrhage (ICH).
  • Regarding hemostatic therapy, new/revised recommendations from the 2007 AHA/ASA guidelines include:
    • Patients with severe thrombocytopenia or factor deficiency should receive platelets or factor replacement
    • Patients with ICH due to oral anticoagulants (warfarin) should receive intravenous vitamin-K and vitamin-K dependent factor replacement
      • Prothrombin complex concentrates (PCCs) are being increasingly used and are considered a reasonable alternative to FFP.  To date, studies have not shown improved outcome with PCCs.
      • Recombinant factor VIIa (rFVIIa) is not recommended as a sole agent for warfarin-related ICH
    • rFVIIa is not recommended in unselected patients
    • Usefulness of platelet transfusions for patients using antiplatelet medications is unclear and currently investigational.

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Drug-Induced Hypophosphatemia

  • Hypophosphatemia is seen in almost 30% of critically ill patients.
  • As discussed in a prior pearl, hypophosphatemia can result in respiratory failure along with cardiac and neurologic abnormalities.
  • Although common ED causes of hypophosphatemia include sepsis, hypothermia, and dialysis, don't forget about medications.
  • Medications that can cause significant hypophosphatemia in the critically ill (along with their mechanism) include:
    • Decreased GI intake: antacids, sucralfate
    • Transcellular shift: aspirin overdose, albuterol, catecholamines, insulin, and bicarbonate
    • Increased urinary excretion: diuretics, acetaminophen overdose, and theophylline overdose

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Hypocapnia and Brain Injury

  • Hypocapnia indirectly reduces cerebral blood volume through reductions in arterial cerebral blood flow.
  • Despite its continued and frequent use, hypocapnia can actually aggravate cerebral hypoxia through reductions in oxygen supply and increases in cerebral oxygen demand.
  • In addition to inducing further cerebral injury, hypocapnia can cause deleterious effects on the heart, lung, and GI tract.
  • To date, there is no evidence that hypocapnia improves outcome in patients with traumatic brain injury or acute stroke.
  • Induced hypocapnia in critically ill ED patients with acute brain injury should primarily be reserved for those with imminent brain herniation.

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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, MBA, MD (Emailed: 7/20/2010) (Updated: 8/14/2024)
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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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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, MBA, MD (Updated: 8/14/2024)
Click here to contact Mike Winters, MBA, MD

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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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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