Tuesday, September 21, 2010

ICU Rounds Report - Sept 21st 2010

September 21st, 2010

Fever. What's your definition of fever? The IDSA (Infectious Disease Society of America) and ACCCM (American College of Critical Care Medicine) say in the ICU it is anything greater than 38.3 (high fever is >39.5). Obviously that doesn't apply to immunocompromised patients. In a mixed ICU group, nearly halve of admissions will get a fever. For our surgical patients, it appears the number is about 75%. All new fevers need a workup and about half of all fevers are eventually found to be non-infectious. Surprisingly, in a series of over 24,000 ICU admissions, fever appears to not affect mortality (because it was so common?). There is a mortality difference among those with high (>39.5) fever and normal or no fever, however (20 vs 12%, P<0.05).

Apart from chasing and managing the etiology, should we treat the fever per se? Probably not, except for head injured patients or those with severe fevers >41C. The biggest trial to date on the issue randomized 86 non-head injured trauma ICU patients from 3 ICUs to Tylenol/cooling blankets vs allowing fevers to run (and treat only if they got to > 40 C). The trial was stopped early because of a trend towards death in the group being treated. (7 deaths vs one in the non-treatment group, p = 0.06) and suggests that treatment of fever may be detrimental in trauma ICU patients. A similar but smaller trial in surgical ICU patients found no difference in outcome. My bias? Let it ride...
O'Grady, NP, Barie, PS, Bartlett, JG, et al. Guidelines for evaluation of new fever in critically ill adult patients: 2008 update from the American College of Critical Care Medicine and the Infectious Diseases Society of America. Crit Care Med 2008; 36:1330.
Laupland, KB, Shahpori, R, Kirkpatrick, AW, et al. Occurrence and outcome of fever in critically ill adults. Crit Care Med 2008; 36:1531.
Gozzoli, V, Schottker, P, Suter, PM, Ricou, B. Is it worth treating fever in intensive care unit patients? Preliminary results from a randomized trial of the effect of external cooling. Arch Intern Med 2001; 161:121.
Schulman, CI, Namias, N, Doherty, J, et al. The effect of antipyretic therapy upon outcomes in critically ill patients: a randomized, prospective study. Surg Infect (Larchmt) 2005; 6:369.

Testing for HITT. Heparin induced thrombocytopenia and thrombosis (type 2, the clinically relevant type) remains a challenge to diagnosis. There are 3 tests used clinically, all are sendouts at UVa. Up to 3% of patients treated with heparin will go on to develop HITT.

1) Serotonin Release Assay. The gold standard. Normal platelets are radiolabeled with serotonin then mixed with patient serum and heparin in different concentrations. Basically if, in the presence of heparin, the serum's antibodies causes the normal platelets to leak serotonin the test is positive. Advantages: This is the only test with good specificity (95%) and sensitivity (95%). Downsides: this test is expensive, tough to perform (takes a week) and is a send out.

2) Heparin induced platelet aggregation. Again healthy donor platelets are mixed with patient serum in the presence of heparin. To have HITT, patients must cause aggregation of the donor platelets in the presence of clinically relevant heparin concentrations. This test is specific (<90%) but not sensitive. It is a slow and a sendout.

3) ELISA Immunoassay. (Called Platelet AB, Heparin-induced at UVa) For many hospitals (not this one) it is done in house. Unlike the top two, this is not a functional assay but simply a look to see if the patient antibodies are present. This is done by mixing patient serum with known heparin antigens and running an ELISA. It is highly sensitive - so it's good at ruling out. Since most of our patients have low pretest probability, this is a good first choice. It's not specific, though so if it comes back positive, it is worth considering a confirmatory test (either of the above). It is a the quickest test to come back (usually 2-3 business days).
Arepally, GM, Ortel, TL. Clinical practice. Heparin-induced thrombocytopenia. N Engl J Med 2006; 355:809.

Continuous Renal Replacement Therapy and Thrombocytopenia. It seems like patients on continuous renal replacement therapies (CRRTs) often have low platelet counts. Coincidence? Nope. Many trials have found that platelet counts and platelet functional ability both drop with CRRT. Concominant HITT? Maybe, but extremely unlikely. A retrospective study published in 2008 showed that one third of patients who received CRRT with concurrent heparin had a greater than 50% decrease in platelet count from baseline and a platelet count less than 100,000/mm3. Almost all these patients were not judged to have HITT.
Holmes et al. The clinical diagnosis of heparin-induced thrombocytopenia in patients receiving continuous renal replacement therapy. Journal of Thrombosis and Thrombolysis. 2008. Volume 27, Number 4, 406-412
Boldt J. Continuous hemofiltration and platelet function in critically ill patients. Crit Care Med. 1994 Jul;22(7):1155-60.

From Danielle
Autonomic Dysreflexia (AD). An uncontrolled sympathetic responses in patients with spinal cord injuries (SCI), is suspected to affect around 50-70% SCI patients with T6 or higher lesions. The primary component is a severe elevation in blood pressure, but other signs and symptoms include headache, flushing, and blotching of skin above the level of the lesion. Most likely, signs and symptoms of AD are due to an imbalance between the parasympathetic pathways above the spinal cord lesion and sympathetic pathway below the spinal cord lesion. Any number of events can trigger AD. They include surgery, anesthesia, bladder distention, urinary tract infections, genital stimulation, GU or GI manipulation, constipation, fractures, skin ulcerations, pregnancy and labor.

Many non-randomized studies have looked at ways to prevent AD. Most studies have focused on preventing the occurrence or autonomic nervous system's detection of GU triggers that cause AD. For example, botulinum toxin maybe be injected into the detrusor muscle to provide relief from bladder distention. Perhaps more importantly, it might be effective to do epidural or nerve blocks during procedures to reduce the occurrence of AD during urological procedures or labor.

Treatment of AD involves managing the triggers that cause episodes and when necessary, pharmaceutical management of elevated blood pressure. Studies have not been done to see which anti-hypertensive medications are most effective. The body of evidence is primarily based on case reports and extrapolation of hypertensive crisis management in patients without spinal cord injuries. In general, there is a consensus to use short acting, rapid onset, anti-hypertensives such as nifedipine which has been reported numerous times to lower blood pressure and control AD episodes. Alpha blockers have had mixed results when used, but sildenafil and captopril have been effective in some case reports.
Krassioukov, et. al. (2009). "A Systematic Review of the Management of Autonomic Dysreflexia After Spinal Cord Injury." Arch. Phys. Med. Rehabil. 90:682-696.

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