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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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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The question of hyperglycemia in the critically ill and how to address it has been the topic of considerable study over the years.

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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• 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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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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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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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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Red blood cell transfusion in the critically ill patient has been and continues to be surrounded by controversy and lack of hard data.  Up to 90 percent of transfusions in the ICU are given for anemia, an indication which is least supported by the data.  The joint taskforce of EAST, ACCM and SCCM has published a clinical practice guideline which outlines recommendations and rationale.  These recommendations are summarized as follows:

• RBC transfusion is indicated for patients with evidence of hemorrhagic shock.
   
• RBC transfusion may be indicated for patients with acute hemorrhage and hemodynamic instability or inadequate DO2.
   
• Transfusion triggers for Hb<7 are as effective as those for Hb<10 in hemodynamically stable critically ill patients, except for those with AMI or USA.
   
• Hb used as a sole trigger is not advised; transfusion decisions should be based on intravascular volume status, evidence of shock, duration and extent of anemia, and cardiopulmonary physiologic parameters.
   
• Consider RBC transfusion if Hb<7 in resuscitated critically ill patients, patients who are being mechanically ventilated or critically ill patients with stable cardiac disease.
   
• RBC transfusion should not be considered as an absolute method to improve tissue oxygen consumption in critically ill patients.
   
• RBC transfusion may be beneficial in patients with acute coronary syndromes with Hb<8 on hospital admission.

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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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Calciphylaxis is a rare disorder caused by systemic arteriolar calcification which leads to ischemia and necrosis.  It is characterized by painful ischemic necrotic lesions on adipose tissue areas such as abdomen, buttock and thighs.  This commonly occurs in patients with ESRD on hemodialysis or after transplant, but can also occur with other patients, such as those with hyperparathyroidism.

Diagnosis is made clinically, with the help of a skin biopsy as needed.  Differential diagnosis includes cholesterol embolization, warfarin necrosis, cryoglobulinemia, cellulitis and vasculitis.  There are no specific laboratory findings, although patients may manifest elevated PTH, phosphorous, calcium or calcium x phosphorous product. 

Infection is usually the cause of the high mortality rate of this condition, which has a reported mortality of 46%, or 80% if ulceration is present.

Treatment includes local wound care, trauma avoidance, electrolyte correction, increased frequency of dialysis or parathyroidectomy as needed.  Surgical debridement is controversial; as the risk of infection may outweigh the benefit in terms of outcome. 

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There is no prospective, randomized study to elucidate propofol’s effect on the critically ill patient. By definition, Propofol Infusion Syndrome (PRIS) has the following characteristics:

• acute bradycardia progressing to asystole
• lipemic plasma
• fatty liver enlargement
• metabolic acidosis with negative base excess > 10
• rhabdomyolysis or myoglobinuria

It has been thought that PRIS was limited to patients with prolonged use, but we now know that this is not necessarily true.

It has been shown that PRIS is more likely with the following risk factors:

• <19 years old
• male
• received a vasopressor
• cardiac manifestations (including Brugada Syndrome)
• metabolic acidosis
• renal failure
• hypotension
• rhabdomyolysis
• dyslipidemia

The treatment for suspected PRIS is:

• Stop infusion
• Hemodynamic stabilization
• Carbohydrate substitution
• Hemodialysis or hemofiltration
• ECMO as necessary

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Severe Acute Pancreatitis

• Patients with acute pancreatitis are considered to have severe acute pancreatitis (SAP) if they manifest signs of shock, respiratory failure, renal faliure, or GI bleeding.
• SAP is almost universally associated with pulmonary dysfunction, typically manifested as an S_pO₂ < 90% in the first few hours of illness.
• In fact, ARDS develops in at least one-third of patients with SAP.
• Take Home Point: Pay close attention to the patient with acute pancreatitis and a low pulse oximetry reading, as many will rapidly deteriorate from ARDS. In those who deteriorate, early intubation with implementation of lung protective ventilatory strategies is indicated.

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Hypoxemia in the Intubated Asthmatic

• Intubating and mechanically ventilating the asthmatic patient can be frought with potential complications that markedly increase morbidity and mortality.
• In the ventilated asthmatic who develops persistent or worsening hypoxemia, evaluate the patient for the following complications:
  • right main stem intubation
  • pneumothorax
  • ETT displacement
  • ETT obstruction
  • air leak around the ETT
  • gastric distention (decreases respiratory system compliance)
  • ventilator malfunction
  • progressive bronchospasm

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This week's pearl is courtesy of Dr. Evie Marcolini.  Thanks Evie!

Abdominal Compartment Syndrome in Burn Patients

• Patients who receive > 250 ml/kg of fluid in the the 24 hours after burn injury will most likely require abdominal decompression.
• In light of this, bladder pressure monitoring should be part of your practice in resuscitation of the patient with >30% TBSA burns.
• The simple act of placing the bladder probe will increase awareness of the possibility of ACS and prompt measurement of abdominal compartment pressures. 
• ACS can be treated with decompressive laparotomy, or in some cases, percutaneous abdominal decompression.

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Extracorporeal Membrane Oxygenation

• In last week's pearl pertaining to critically ill patients with H1N1, I mentioned the use of ECMO as a potentially life-sustaining treatment for refractory respiratory failure.
• Essentially, ECMO removes blood from the patient and circulates it through an artificial lung with a pump.  For patients with respiratory failure, this is usually accomplished via cannulation of the femoral and internal jugular veins.
• General guidelines to consider ECMO in severe, refractory respiratory failure include:
  • P_aO₂ / F_iO₂ ratio < 100 on 100% F_iO₂ or A-a gradient > 600 mm Hg
  • Age < 65 years
  • No known contraindication to anticoagulation
  • Lack of significant co-morbidities (due to prolonged recovery after weaning from ECMO)

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Critically Ill Patients with H1N1

• Three recent reports published online in the Journal of the Americal Medical Association (JAMA) detail the potential problems of H1N1 infection in the critically ill.
• The three studies (Mexico, Canada, Australia/New Zealand) seem to have recurring themes:
  • shock and multisystem organ failure were common
  • many were healthy, young adults who developed rapid respiratory failure
  • hypoxemia was prolonged and often refractory to conventional modes of mechanical ventilation
• Newer modes of ventilation and therapies were required to treat refractory hypoxemia.  These included high frequency oscillatory ventilation, prone positioning, neuromuscular blockade, nitric oxide, and extracorporeal membrane oxygenation.
• Take Home Point: Involve your intensivist early in the management of ED patients with respiratory failure and suspected H1N1 infection, as non-conventional methods of ventilation may be needed to treat hypoxemia.

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