Category: Critical Care
Posted: 6/22/2010 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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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.
Rinaldo Bellomo1, Claudio Ronco, John A Kellum, Ravindra L Mehta, Paul Palevsky and the ADQI workgroup
Acute Renal Failure - definition, outcome measures, animal models, fluid therapy and information technology needs: The Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group.
Critical Care 2004, 8:R204-R212 (DOI 10.1186/cc2872)
This article is online at: http://ccforum.com/content/8/4/R204
Category: Critical Care
Posted: 6/1/2010 by Evadne Marcolini, MD
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Marino P. The ICU Book. 3rd ed. Lippincott
Category: Critical Care Literature Update
Posted: 5/18/2010 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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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!
Marchik, MR et al. The Significance of Non-sustained Hypotension in Emergency Department Patients with Sepsis.Intensive Care Medicine (2009) 35:1261-1264
Category: Critical Care
Posted: 5/3/2010 by Evadne Marcolini, MD
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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:
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
Fink MP, Abraham E, Vincent JL, Kochanek PM, eds. Textbook of Critical Care. 5th ed. Philadelphia, PA: Elsevier/Saunders; 2005.
Category: Critical Care
Posted: 4/20/2010 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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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.
Paolini JM et al: Predictive value of abdominal obesity vs. body mass index for determining risk of intensive care unit mortality. Crit Care Med 2010; 38:1-7
Category: Critical Care
Posted: 4/6/2010 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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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.
Marino P. The ICU Book. 3rd ed. Lippincott Williams & Wilkins, 2007:625-638.
Category: Critical Care
Posted: 3/23/2010 by Evadne Marcolini, MD
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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
Frasca D, Dahyot-Fizelier C, Mimoz O: Prevention of central venous catheter-related infection in the intensive care unit. Crit Care; 2010; 14:212
Karakitsos D, Labropoulos N, De Groot E: Real time ultrasound guided catheterisation of the internal jugular vein: A prospective comparison with the landmark technique in critical care patients. Crit Care 2006; 10(6):175.
Category: Critical Care
Posted: 3/5/2010 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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Primary Intracranial hemorrhage is associated with the following risk factors:
Common causes of secondary ICH are as follows:
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
Nyquist P: Management of Acute Intracranial and Intraventricular Hemorrhage. Crit Care Med 2010;38(3):946-953
Category: Critical Care
Posted: 2/22/2010 by Evadne Marcolini, MD
(Updated: 2/23/2010)
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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.
Flaciglia M, Freyberg RW et al: Hyperglycemia-related mortality in critically ill patients varies with admission diagnosis. Crit Care Med 2009;37:3001-3009
Category: Critical Care
Posted: 2/3/2010 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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There are several conditions that alter ionized calcium levels, including:
The bottom line is to measure ionized calcium, and consider all other factors that can be contributing to hypocalcemia in addition to repleting it.
Category: Critical Care
Posted: 1/26/2010 by Evadne Marcolini, MD
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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:
Treatment of HIT:
Critical Care Med 2010 Vol. 38, No. 2 (Suppl.)
Category: Critical Care
Posted: 1/12/2010 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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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.
Category: Critical Care
Posted: 12/28/2009 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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Category: Critical Care
Posted: 12/15/2009 by Evadne Marcolini, MD
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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:
Napolitano LM et al: Clinical practice guideline: Red blood cell transfusion in adult trauma and critical care: Crit Care Med 2009;37:3124-3157
Category: Critical Care
Posted: 11/30/2009 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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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.
Reference:
Category: Critical Care
Posted: 11/17/2009 by Evadne Marcolini, MD
(Updated: 12/9/2024)
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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:
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:
The treatment for suspected PRIS is:
Fudickar A, Bein B Propofol infusion syndrome: update of clinical manifestation and pathophysiology. Minerva Anestesiologica 2009;75:339-44.
Vernooy K, Delhaas T, et al. Electrocardiographic changes predicting sudden death in propofol-related infusion syndrome. Heart Rhythm 2006;3:131-7