UMEM Educational Pearls - Critical Care

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: 12/9/2019)
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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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In the ICU, diabetes insipidus (DI) develops in patients with pituitary surgery, brain trauma, intracranial hypertension and brain death.  Criteria include the following:

  • urine output >200 ml/hr or 3 ml/kg/hr
  • urine osmolality <150 mOsm/kg
  • serum sodium>145 mEq/L
  • urine specific gravity<1.005

In the ICU, patients are typically unable to consume free water to compensate for urinary losses, and dehydration, hypotension and hypernatremia occur.  Clinical signs may not appear until sodium levels surpass 155-160 mEq/L or serum osmolality surpsses 330 mOsm/kg. 

Symptoms include confusion, lethargy, coma, seizures and cerebral shrinkage associated with subdural or intraparenchymal hemorrhage. 

Treatment includes

  • controlling polyuria with vasopressin (antidiuretic, vasoconstrictive effects) and desmopressin (DDAVP - antidiuretic effect)
  • calculate and replace free water loss
  • TBW deficit (L) = body weight (kg) x 0.6 x (Na-140)/Na
  • monitor and replace urine losses hourly (using gastric access if possible)
  • monitor serum sodium and adjust therapy every 4 hours closely monitor for hyperglycemia and treat to prevent osmotic diuresis due to glucosuria

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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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It is true, 1/3 of Americans are obese.  There is conflicting evidence regarding the mortality risk of obesity (defined as BMI>30 kg/m2) in critically ill patients. 

It has been shown that abdominal fat has greater consequences than peripheral obesity, and based on this, a recent study has utilized the sagittal abdominal diameter (SAD) in ICU patients to show that abdominal obesity (as differentiated from BMI) poses an independent risk of death.  The SAD detects visceral fat, which has been shown to have metabolic and immune health consequences, including the following:

-incidence and severity of certain infections is higher

-excess adipocytes are associated with elevated levels of proinflammatory factors that favor insulin resistance, diabetes, dyslipidemia and hypertension, all of which lead to microcirculatory dysfunction

-rates of required renal replacement therapy and abdominal compartment syndrome correlate to increased SAD

-there is also a trend toward a longer length of ventilator weaning

See you at the gym.

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Category: Critical Care

Title: Type B Lactic Acidosis

Posted: 4/13/2010 by Mike Winters, MD (Updated: 12/9/2019)
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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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Category: Critical Care

Title: Magnesium Balance

Posted: 4/6/2010 by Evadne Marcolini, MD (Updated: 12/9/2019)
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Magnesium depletion has been described as "the most underdiagnosed electrolyte abnormality in current medical practice"

Important for electrically excitable tissues and smooth muscle cells, Mg is mostly located in bone, muscle and soft tissue.  Because only 1% is located in blood, your patient can be Mg depleted with normal serum levels. 

65% of ICU patients are magnesium depleted (and may not be hypomagnesemic). Because labs are unreliable, consider predisposing causes, such as diuretics, antibiotics (aminoglycosides, amphotericin), digitalis, diarrhea, chronic alcohol abuse, diabetes and acute MI (80% of AMI patients will have magnesium depletion in the first 48 hours). 

Mg depletion is typically accompanied by depletion of other electrolytes (K, Phos, Ca), and can cause arrhythmias (especially torsades) and promote digitalis cardiotoxicity. 

Hypermagnesemia is less common, and can be caused by hemolysis, renal insufficiency, DKA, adrenal insufficiency and lithium toxicity.  Clinical findings include hyporeflexia, prolonged AV conduction, heart block and cardiac arrest.  Treatment includes fluid and furosemide, calcium gluconate and dialysis. 

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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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Catheter-related bloodstream infections occur in 3-8 percent of insertions, and are the highest cause of nosocomial bloodstream infections in the ICU. 

The most effective measures to prevent catheter-related infections are as follows:

Especially applicable to those of us placing these lines in the ED or in the ICU is the last recommendation, based on a prospective study from Greece

-adequate knowledge and use of care protocols

-qualified personnel involved in changing and care

-use of biomaterials that inhibit microorganism growth and adhesion

-good hand hygiene

-use of an alcoholic formulation of chlorhexidine for skin disinfection and manipulation of the vascular line

-preference for subclavian route for placement

-use of full barrier protection during placement

-removal of unnecessary catheters

-use of ultrasound for placement of central lines

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Category: Critical Care

Title: Warfarin and ICH

Posted: 3/16/2010 by Mike Winters, MD (Updated: 12/9/2019)
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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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Primary Intracranial hemorrhage is associated with the following risk factors:

  • hypertension, smoking, alcohol, hypocholesterolemia, genetic factors, warfarin, phenylpropylamine, cocaine and methamphetamine. 

Common causes of secondary ICH are as follows:

  • vascular malformations, arteriovenous malformations, cavernous angiomas, small arterial telangiectasia, and primary and secondary brain tumors.

The question of how to address elevated blood pressure in spontaneous intracranial hemorrhage has been debated.  High blood pressure may cause hematoma expansion, but this has not been proven.  Lowering blood pressure may help reduce neurologic deterioration, but this has also not been proven in the literature. 

The AHA recommended guidelines for blood pressure management in spontaneous ICH are as follows:

If SBP>200 or MAP>150, consider aggressive reduction of BP with continuous IV infusion, monitoring BP every 5 minutes

If SBP>180 or MAP>130, with evidence or suspicion of elevated ICP, consider monitoring ICP and reducing BP using intermittent or continuous IV medications to keep CPP>60 to 80

If SBP>180 or MAP>130 without evidence or suspicion of elevated ICP, then consider a modest reduction of BP (MAP of 110 or targeted SBP 160/90) using intermittent or continuous IV medications, monitoring BP every 15 minutes

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Category: Critical Care

Title: Vent Strategies for TBI

Posted: 3/2/2010 by Mike Winters, MD (Updated: 12/9/2019)
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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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Category: Critical Care

Title: Hyperglycemia

Posted: 2/22/2010 by Evadne Marcolini, MD (Emailed: 2/23/2010) (Updated: 2/23/2010)
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There have been several attempts to try to quantify the best target glucose levels in critically ill patients.  This is still a moving target, but a recent study sheds some light on the effect of different levels of hyperglycemia and the types of patients who are particularly vulnerable.

This is a retrospective cohort study whic reviewed 259,000 ICU admissions over a three year period at 173 separate sites.  Their findings were as follows:

Compared with normoglycemic patients, the adjusted odds for mean glucose 111-145, 146-199, 200-300, and >300 was 1.31, 1.82, 2.13 and 2.85 respectively.

There is a clear association between the adjusted odds of mortality related to hyperglycemia in patients with AMI, arrhythmia, unstable angina, pulmonary embolism, pneumonia and gastrointestinal bleed.

Hyperglycemia associated with increased mortality was independent of type of ICU, length of stay and/or pre-existing diabetes.

So, even though we have not come to solid conclusions about how far down to keep the glucose levels down, it makes sense to pay particular attention and be more vigilant of the blood glucose levels, especially in the higher-risk patients  listed above. 

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Category: Critical Care

Title: Hypocalcemia

Posted: 2/3/2010 by Evadne Marcolini, MD (Emailed: 2/9/2010) (Updated: 12/9/2019)
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  • Total body calcium consists of about half biologically active (ionized) and half inactive (80% bound to albumin and 20% to other ions)
  • hypocalcemia caused by hypoalbuminemia is physiologically insignificant, and correction factors are not accurate or reliable
  • The best way to measure true active calcium is to order an ionized calcium level

There are several conditions that alter ionized calcium levels, including:

  • alkalosis (increases binding to albumin)
  • gas bubbles in the sample (false lowering of calcium)
  • anticoagulants (must be collected in a red top tube)
  • blood transfusions (binding to citrate)
  • cardiopulmonary bypass
  • drugs (aminoglycosides, cimetidine, heparin, theophylline)
  • fat embolism
  • hypomagnesemia (correcting mg levels may preclude need for Ca repletion)
  • pancreatitis (several mechanisms, poor prognosis)
  • renal insufficiency (impaired phosphate retention)
  • sepsis

The bottom line is to measure ionized calcium, and consider all other factors that can be contributing to hypocalcemia in addition to repleting it. 

 

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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Patients in the Critical Care setting may develop HIT as a result of chronic pre-existing risk factors (malignancy, obesity, hypertension, diabetes or medications) or acquired factors secondary to their ICU stay (post-operative state, trauma, central lines or medications such as heparin).

Diagnosis of HIT:

  • platelet count<150,000 or relative decrease of 50% or more from baseline
  • documentation of antibodies binding platelet factor 4 and heparin, as well as a confirmation test
  • typically occurs 5-14 days after initiation of heparin therapy
  • can have a rapid (usually a result of previous exposure) or delayed onset
  • thrombotic complications develop in 20-50 percent of patients

Treatment of HIT:

  • Remove all sources of heparin (including heparin-bonded catheters)
  • initiate a non-heparin anticoagulant
  • Direct thrombin inhibitors:
    • Lepirudin (cleared by kidney)
    • Argatroban (cleared by liver)
    • Bivalirudin (cleared by proteolysis 80% and kidney 20%)
  • Other agents used include:
    • Danaparoid (antifactor Xa activity - not available in North America)
    • Fondaparinux (synthetic selective inhibitor of Xa)

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Category: Critical Care

Title: Defining AKI

Posted: 1/19/2010 by Mike Winters, MD (Updated: 12/9/2019)
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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: Sepsis Definition

Posted: 1/12/2010 by Evadne Marcolini, MD (Updated: 12/9/2019)
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The term Sepsis is frequently and colloquially used to describe "sick" patients; but accuracy requires understanding the specific criteria of Sepsis and its associated syndromes.  Following are the defining criteria for SIRS and Sepsis:

SIRS

at least 2 of the following:

Temp >38C or <36C

Heart rate >90

RR> 20 or pCO2<32mm Hg

WBC>12,000, <4,000 or >10% bands

 

Sepsis:

Systemic response to infection, manifested by 2 or more SIRS criteria with a source of infection confirmed by culture or a clinical syndrome pathognomic for infection.


Severe Sepsis:

Sepsis associated with acute organ dysfunction, hypoperfusion or hypotension; including lactic acidosis, oliguria or altered mental status.


Septic Shock:

Sepsis-induced hypotension not responsive to fluid resuscitation.

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Category: Critical Care

Title: AKI and the Critically Ill

Posted: 1/5/2010 by Mike Winters, MD (Updated: 12/9/2019)
Click here to contact Mike Winters, MD

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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ICU patients commonly exhibit altered mental status(AMS), which may be due to any of several factors.  For those who do not have head injury, below are the most common etiologies of AMS:
 
-Stroke/hemorrhage, post cardiac arrest, encephalitis, seizure, hypo/hyperthermia
 
-Drug or ETOH withdrawl, thiamine deficiency, water intoxication, toxins
 
-Hyperthyroid (apathetic), hypothyroid
 
-Medications, line sepsis
 
-Decreased pO2, increased pCO2, ARDS, pneumonia
 
-Heart failure, hyper/hypotension
 
-Hepatic failure, biliary sepsis
 
-Hyper/hypoglycemia, pancreatitis
 
-Adrenal insufficiency
 
-Renal failure, urosepsis, post-dialysis electrolyte imbalance (Na, Ca, PO4)
 
-Fat embolism
 
Ischemic stroke has been shown to be the most frequent cause of AMS on admission to the ICU, and septic encephalopathy the most commmon cause of AMS developing after admission to the ICU. 

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