Title: Drug-Induced Hypophosphatemia

Category: Critical Care

Posted: 8/10/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Hypocapnia and the Injured Brain

Category: Critical Care

Posted: 8/3/2010 by Mike Winters, MBA, MD

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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Title: Drug Induced Thrombocytopenia in the Critically Ill

Category: Critical Care

Posted: 7/27/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: ICU Acquired Weakness

Category: Critical Care

Posted: 7/20/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Drug-Drug Interactions in the Critically Ill

Category: Critical Care

Posted: 7/13/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Asthma, Peak Pressures, and the Ventilator

Category: Critical Care

Posted: 7/6/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Acidosis and Intubation

Category: Critical Care

Posted: 6/29/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Hypotension and MV

Category: Critical Care

Posted: 6/15/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Platelet Transfusions in the Critically Ill

Category: Critical Care

Posted: 6/8/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: PCAS: Controlled Reoxygenation

Category: Critical Care

Posted: 5/25/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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 F_iO₂ to maintain S_pO₂ of 94-96%
- Avoid unnecessary arterial hyperoxia

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Title: PRBCs in Neurocritical Care

Category: Critical Care

Posted: 5/11/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: PRBCs in the Critially Ill Patient with Cardiac Disease

Category: Critical Care

Posted: 4/27/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Type B Lactic Acidosis

Category: Critical Care

Posted: 4/13/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: H1N1 Ventilator Pearls

Category: Critical Care

Posted: 3/30/2010 by Mike Winters, MBA, MD

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 F_iO₂ to maintain S_pO₂ > 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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Title: Warfarin and ICH

Category: Critical Care

Posted: 3/16/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Vent Strategies for TBI

Category: Critical Care

Posted: 3/2/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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 P_aO₂ > 60 mm Hg, most suggest a higher P_aO₂ (> 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 P_aCO₂ 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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Title: Ultrasound in the Critically Ill

Category: Critical Care

Posted: 2/2/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Defining AKI

Category: Critical Care

Posted: 1/19/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: AKI and the Critically Ill

Category: Critical Care

Posted: 1/5/2010 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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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Title: Appropriate Antibiotics in Sepsis

Category: Critical Care

Posted: 12/22/2009 by Mike Winters, MBA, MD (Updated: 10/20/2026)

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.

201-220 of 356 results by Mike Winters

Title: Drug-Induced Hypophosphatemia

Title: Hypocapnia and the Injured Brain

Title: Drug Induced Thrombocytopenia in the Critically Ill

Title: ICU Acquired Weakness

Title: Drug-Drug Interactions in the Critically Ill

Title: Asthma, Peak Pressures, and the Ventilator

Title: Acidosis and Intubation

Title: Hypotension and MV

Title: Platelet Transfusions in the Critically Ill

Title: PCAS: Controlled Reoxygenation

Title: PRBCs in Neurocritical Care

Title: PRBCs in the Critially Ill Patient with Cardiac Disease

Title: Type B Lactic Acidosis

Title: H1N1 Ventilator Pearls

Title: Warfarin and ICH

Title: Vent Strategies for TBI

Title: Ultrasound in the Critically Ill

Title: Defining AKI

Title: AKI and the Critically Ill

Title: Appropriate Antibiotics in Sepsis