UMEM Educational Pearls - By Evadne Marcolini

Acute renal failure occurs in 1-25% of critically ill patients, with an associated mortality of 28 - 90%. 

The RIFLE Criteria represent the first consensus definition of acute renal failure used to classify critically ill patients as to their kidney function.  Notably, we use the worst possible classification according to the criteria, which measures either serum creatinine, urine output or both. 

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Neuroleptic malignant syndrome (NMS), which is similar in symptomatology to malignant hyperthermia (MH), is characterized by the following:
1) increased body temperature
2) muscle rigidity
3) altered mental status
4) autonomic instability
 
The difference between NMS and MH is the etiology.  NMS is caused by the following medications:
Antipsychotics (haldol, phenothiazines, clozapine, olanzapine, risperadone)
Antiemetics (metoclopramide, droperidol, prochlorperazine)
CNS stimulants (amphetamines, cocaine)
Other (lithium, TCA overdose)
 
NMS can also be cause by disconinuation of dopaminergic drugs (amantadine, bromocriptine, levodopa)
 
Symptoms can begin to appear 24 to 72 hours after the onset of drug therapy, and are usually gradual. 
 
Management includes checking CK level (>1000 distinguishes NMS from sepsis), immediate removal of the offending drug, and consideration of Dantrolene or Bromocriptine.

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A single episode of hypotension portends a worse outcome for septic patients.  The restrospective analysis by Marchick et al of 700 patients showed that mortality was 10% vs 3.6% for septic patients whose SBP dropped below 100 even once.  It was also noted that the lower the SBP, the worse the in-hospital mortality.

So, not only do we need to remember to watch blood pressure closely for head-injured patients, but for septic patients as well!

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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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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: Magnesium Balance

Posted: 4/6/2010 by Evadne Marcolini, MD (Updated: 11/27/2020)
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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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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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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: 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: 11/27/2020)
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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. 

 

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: Sepsis Definition

Posted: 1/12/2010 by Evadne Marcolini, MD (Updated: 11/27/2020)
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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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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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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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Category: Critical Care

Title: Calciphylaxis

Posted: 11/30/2009 by Evadne Marcolini, MD (Emailed: 12/1/2009) (Updated: 11/27/2020)
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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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