Abstract of Current management of Septic Shock. Read here...
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Showing posts with label Intensive care. Show all posts
Showing posts with label Intensive care. Show all posts
Septic Shock
November 15, 2008
Posted by arif at 7:17 PM View Comments
Labels: Infectious disease, Intensive care
Move to top of post.Antifungals in ICU
September 5, 2008
In critically ill adults with risk factors for invasive candidiasis, empirical fluconazole did not clearly improve a composite outcome more than placebo. Study reported in Annals of Internal Medicine..
Tight Control Is Not Necessary in ICU
September 1, 2008
Risks of Tight Glucose Control in ICU May Outweigh Benefits
Against conventional wisdom, tight glucose control in critically ill patients has not reduced in-hospital death rates. Instead, according to a meta-analysis here, it increases the risk of hypoglycemic episodes.
With data pooled from 27 randomized trials involving 8,315 patients, the relative risk of hospital mortality was 0.93 (95% CI 0.85 to 1.03) for tight glucose control versus usual care, reported Renda Soylemez Wiener, M.D., M.P.H., of the VA Medical Center here, and colleagues in the Aug. 27 issue of the Journal of the American Medical Association.
The American Diabetes Association and several other medical societies have recommended tight glucose control for all critically ill patients, mainly on the basis of a 2001 study that found it reduced hospital mortality among critically ill surgical patients by one-third, said Dr. Wiener and colleagues.
"Subsequent large randomized controlled trials of tight glucose control in medical and mixed medical-surgical ICU settings, however, have failed to replicate this mortality benefit," the researchers said, prompting them to undertake the systematic review.
In an interview, Dr. Wiener said the meta-analysis results warrant a re-evaluation of recommendations of tight glucose control for all ICU patients.
Tight glucose control generally means seeking to keep blood glucose below 150 mg/dL with an insulin infusion during some or all of the ICU stay. Some guidelines, including those endorsed by the ADA, call for glucose levels of 80 to 110 mg/dL.
This study does not surprise me. Achieving tight control while providing intensive care does not have an obvious biologic theory. Of course, if glucose is your focus of attention, then you would be attracted to a glucose theory.
Generally patients in an ICU have so many different problems, that achieving balance seems more important than focusing too deeply on one factor.
Against conventional wisdom, tight glucose control in critically ill patients has not reduced in-hospital death rates. Instead, according to a meta-analysis here, it increases the risk of hypoglycemic episodes.
With data pooled from 27 randomized trials involving 8,315 patients, the relative risk of hospital mortality was 0.93 (95% CI 0.85 to 1.03) for tight glucose control versus usual care, reported Renda Soylemez Wiener, M.D., M.P.H., of the VA Medical Center here, and colleagues in the Aug. 27 issue of the Journal of the American Medical Association.
The American Diabetes Association and several other medical societies have recommended tight glucose control for all critically ill patients, mainly on the basis of a 2001 study that found it reduced hospital mortality among critically ill surgical patients by one-third, said Dr. Wiener and colleagues.
"Subsequent large randomized controlled trials of tight glucose control in medical and mixed medical-surgical ICU settings, however, have failed to replicate this mortality benefit," the researchers said, prompting them to undertake the systematic review.
In an interview, Dr. Wiener said the meta-analysis results warrant a re-evaluation of recommendations of tight glucose control for all ICU patients.
Tight glucose control generally means seeking to keep blood glucose below 150 mg/dL with an insulin infusion during some or all of the ICU stay. Some guidelines, including those endorsed by the ADA, call for glucose levels of 80 to 110 mg/dL.
This study does not surprise me. Achieving tight control while providing intensive care does not have an obvious biologic theory. Of course, if glucose is your focus of attention, then you would be attracted to a glucose theory.
Generally patients in an ICU have so many different problems, that achieving balance seems more important than focusing too deeply on one factor.
Quantitative ETA and VAP
August 19, 2008
Our patients admitted for ventilation get Endotracheal aspirate cultured routinely twice a week. Is this practice cost effective? Does this help in identifying the VAP bug or not? Read this editorial...
Role of quantitative endotracheal aspirate and cultures as a surveillance and diagnostic tool for ventilator associated pneumonia: A pilot study
Role of quantitative endotracheal aspirate and cultures as a surveillance and diagnostic tool for ventilator associated pneumonia: A pilot study
Posted by arif at 3:04 PM 0 comments
Labels: Infectious disease, Intensive care
Move to top of post.Sepsis
July 20, 2008
Management of severe sepsis has always been difficult. Treatment of sepsis has gone round in circles from giving steroids and activated protein C. This is review article of diagnosis and management of sepsis published recently.
Read here the full article..
If you have time to read the full supplement published in critical care click here..
Read here the full article..
If you have time to read the full supplement published in critical care click here..
Refeeding Syndrome
July 2, 2008
Posted by arif at 9:59 PM 0 comments
Labels: Intensive care, Internal medicine, Nutrition
Move to top of post.Rhabdomyolysis
June 5, 2008
A 32-year-old man with no significant past medical history presented to the emergency department with complaints of weakness, myalgias, and muscle stiffness. Physical examination was notable for a low-grade fever at 100.8°F, mild tachycardia at 110 bpm, and moderate tenderness on palpation of the muscle groups of the calves, thighs, biceps, triceps, and shoulder girdle. Cardiac auscultation revealed no murmurs, neurologic examination showed no focal deficits, and skin examination was normal. On further questioning, the patient admitted to using crack cocaine for 2 days. Notable laboratory values were as follows: a white blood cell count of 15,000 cells/μL (normal, 4500–11,000 cells/μL), creatine kinase level of 16,500 IU/L (normal, 40–150 IU/L), blood urea
nitrogen level of 29 mg/dL (normal, 8–23 mg/dL), creatinine level of 1.1 mg/dL (normal, 0.6–1.2 mg/dL), and potassium level of 4.0 mEq/L (normal, 40–150 mEq/L). Urine myoglobin was not detected, urinalysis was normal, and urine toxicologic screen was positive for cocaine. Rapid influenza testing was negative. The patient was admitted to the medical floor with a diagnosis of
cocaine-induced rhabdomyolysis.
nitrogen level of 29 mg/dL (normal, 8–23 mg/dL), creatinine level of 1.1 mg/dL (normal, 0.6–1.2 mg/dL), and potassium level of 4.0 mEq/L (normal, 40–150 mEq/L). Urine myoglobin was not detected, urinalysis was normal, and urine toxicologic screen was positive for cocaine. Rapid influenza testing was negative. The patient was admitted to the medical floor with a diagnosis of
cocaine-induced rhabdomyolysis.
This review in Hospital Physician covers important questions in management such as when to alkalinize the urine, when to use mannitol and when to dialyze.
Transfusion Reaction: What every Physician should know
June 1, 2008
Blood transfusion is life saving but every time you transfuse blood you have to remember that various adverse reactions can happen. Successful investigation of a transfusion reaction depends on detailed observation, documentation and reporting of the patient’s vital signs, before and after the transfusion, and the signs and symptoms that prompted the investigation.
This article published in Canadian Journal of Clinical Medicine should read by every hospitalist.
Posted by arif at 3:48 AM View Comments
Labels: Blood transfusion, Intensive care
Move to top of post.Universal screening for MRSA? not primetime Yet
May 25, 2008
Recently, there has been a lot of coverage in press about the “recent” epidemic of methicillin-resistant Staph Aureus (MRSA) infections. In reality, we know that the MRSA epidemic really isn’t new, but it is a huge problem that isn’t improving on its own. So what is the most effective way to reduce MRSA infections?
A study from Northwestern published in the Annals of Internal Medicine examined the outcomes of instituting a comprehensive MRSA screening in a large academic medical system. Starting in Arpil 2004, all patients admitted to an ICU had nasal swabs to test for MRSA colonization (74% adherence). Patients that were positive based on PCR testing were placed on contact isolation. After 12 months of this protocol, the surveillance program was expanded to the entire hospital system. During this phase of the study, patients that tested positive underwent decolonization with muciporin and a chlorhexidine wash/shower (how clean!). The study found a decrease in the incidence of MRSA disease by 70%. Most notably, while there was decreased MRSA surgical site and UTI, there was no statistically significant decrease in MRSA bacteremia with universal surveillance. Also since MRSA is associated with higher mortality, it’s odd that this study did not try to observe for decreased mortality. These results contradict the findings of a recent study published in JAMA that did not find any significant reduction in surgical site infections with universal screening. While this study does not absolutely prove universal MRSA surveillance is ready for primetime, it is a significant step in creating a robust and sensible system to improve our detection and containment of MRSA transmission.
Posted by arif at 8:04 PM View Comments
Labels: Infectious disease, Intensive care, microbiology
Move to top of post.Liver puzzle
May 22, 2008
55 year old man admitted to our service for ascites and anasarca (massive scrotal and leg edema.) The patient had large volume paracentesis. The SAAG (serum ascites albumin gradient) was 1.8 - consistent with portal hypertension. He had no evidence for spontaneous bacterial peritonitis. His serum ammonia was normal. Later that evening he becomes hypoxic and is transferred to intensive care. He is placed on a 50% rebreathing mask. In reviewing his lab data we find: shows:
AST 34 alk phos 98 albumin 2.7 ALT 27 T. Bili. 0.8 INR1.3
pH 7.115 pCO2 91 pO2 90
His ABG the next morning on 50% O2
Arterial Blood Gas - 50% oxygen
When he was admitted he had a serum bicarbonate of 31.
He has cardiomegaly on chest xray.
Questions:
1. What liver diseases might he have - what is your best guess?
2. What other tests would you order?
3. Why is his pCO2 so high?
I will provide some answers and a strong hypothesis.
Why Are Hypotonic Parenteral Fluids Still Being Used?
May 18, 2008
Hospital-acquired hyponatremia can be lethal. There have been multiple reports of death or permanent neurological impairment in both children and adults. The main factor contributing to the development of hospital-acquired hyponatremia is routine use of hypotonic fluids in patients in whom the excretion of free water, which is retained in response to excess arginine vasopressin (AVP), might be impaired. The practice of administering hypotonic parental fluids was established over 50 years ago, before recognition of the fact that there are numerous potential stimuli for AVP production in most hospitalized patients. Virtually all neurological morbidity resulting from hospital-acquired hyponatremia has been associated with administration of hypotonic fluids. Multiple prospective studies have shown that 0.9% NaCl is effective prophylaxis against hyponatremia. There is not a single report in the literature of neurological complications resulting from the use of 0.9% NaCl in non-neurosurgical patients. Patients at greatest risk of developing hyponatremic encephalopathy following hypotonic fluid administration are children, premenopausal females, postoperative patients, and those with brain injury or infection, pulmonary disease or hypoxemia. When hyponatremic encephalopathy develops, immediate administration of 3% NaCl is essential. In this Review, authors discuss the question of why administering hypotonic fluids is unphysiologic and potentially dangerous, the settings in which isotonic fluids should be administered to prevent hyponatremia, and the appropriate treatment of hyponatremic encephalopathy.
Clinical pearls:
Several key points that added to my knowledge:
1. Premenopausal women are more likely to develop hyponatremic encephalopathy - probably secondary to the effect of estrogen on astrocytes - therefore increased cerebral edema for the same level of hyponatremia
2. The cerebral edema can cause non-cardiogenic pulmonary edema - and thus hypoxemia.
3. When hypoxemia occurs, then cerebral blood flow decreases, with potential disastrous results.
4. Author argues passionately against the routine use of hypotonic parenteral fluids
5. Author argues that the treatment for hyponatremic encephalopathy is 100 cc of hypertonic saline (3%) push, with transfer to the ICU and careful frequent monitoring of sodium levels. Pulmonary edema is not a contraindication to hypertonic saline if the patient has normal heart size.
This was truly an excellent review on an infrequent but potentially lethal condition. Author included in the discussion the consideration of marathon runners. He now recommends that marathon runners to present with altered mental status should receive 100 cc of 3%NS bolus.
Posted by arif at 7:05 PM 0 comments
Labels: Electrolyte Disorders, Intensive care, Internal medicine
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