Is it true? Does azithromycin kill people?

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Is it true? Does azithromycin kill people?

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Should you give thrombolytics to patients with diabetes, prior stroke, or both? The conclusions of the authors might lead you astray here.

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Should you give thrombolytics to patients with diabetes, prior stroke, or both? The conclusions of the authors might lead you astray here.

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Does everyone with monoarticular arthritis need arthrocentesis? Check the evidence. ESR and CRP aren't so hot...

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Does everyone with monoarticular arthritis need arthrocentesis? Check the evidence. ESR and CRP aren't so hot...

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Jacobs IG et al. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomized double-blind placebo-controlled trial. Resuscitation 2011;82:1138- 1143.

Context: Epinephrine is considered standard of care for cardiac arrest in kids and adults. Surprisingly, there are no randomized controlled clinical trials that show it is of benefit. We know from past studies that high-dose epinephrine got more patients to the hospital alive, but there was no increase in survival to hospital discharge. What about regular dose of epinephrine?  Is there any evidence for its use?

Abstract Thinking (PubMed)

Background: There is little evidence from clinical trials that the use of adrenaline (epinephrine) in treating cardiac arrest improves survival, despite adrenaline being considered standard of care for many decades.

The aim of our study was to determine the effect of adrenaline on patient survival to hospital discharge in out of hospital cardiac arrest.

Methods: We conducted a double blind randomised placebo-controlled trial of adrenaline in out-of-hospital cardiac arrest. Identical study vials containing either adrenaline 1:1000 or placebo (sodium chloride 0.9%) were prepared. Patients were randomly allocated to receive 1 ml aliquots of the trial drug according to current advanced life support guidelines. Outcomes assessed included survival to hospital discharge (primary outcome), pre-hospital return of spontaneous circulation (ROSC) and neurological outcome (Cerebral Performance Category Score - CPC).

Results: A total of 4103 cardiac arrests were screened during the study period of which 601 underwent randomisation. Documentation was available for a total of 534 patients: 262 in the placebo group and 272 in the adrenaline group. Groups were well matched for baseline characteristics including age, gender and receiving bystander CPR. ROSC occurred in 22 (8.4%) of patients receiving placebo and 64 (23.5%) who received adrenaline (OR = 3.4; 95% CI 2.0-5.6). Survival to hospital discharge occurred in 5 (1.9%) and 11 (4.0%) patients receiving placebo or adrenaline respectively (OR = 2.2; 95% CI 0.7-6.3). All but two patients (both in the adrenaline group) had a CPC score of 1-2.

Conclusion: Patients receiving adrenaline during cardiac arrest had no statistically significant improvement in the primary outcome of survival to hospital discharge although there was a significantly improved likelihood of achieving ROSC.

Comment and Critique: The study design and methodology were sound, and the study was carried out well. However, it has a few problems. It was single-center in western Australia; ambulance response times were a bit slow (mean of ten minutes); and they did not enroll >2200 patients per group as planned. So it is underpowered to detect the primary outcome, namely a 2% increase in survival to discharge (beyond the 5% baseline). They also failed to enroll 906 patients who were eligible, and there was no comment on whether or not the patients missed were significantly different than those enrolled, potentially producing selection bias. In 67 patients the randomization number was lost or not recorded. There is no comment on the use of therapeutic hypothermia while hospitalized. Can we assume neither group received this treatment? Overall, the study showed the superiority of epinephrine in producing ROSC and survival to hospital admission.  It showed a trend toward improved survival to discharge but was underpowered to detect a true difference.

Change in Practice: I think we need to keep epinephrine in our resuscitation protocols. More patients will have ROSC and make it to the hospital. The real question is whether more will make it home neurologically intact, and this study can't answer that.

Further Reading:

Olasveengen TM et al. Intravenous Drug Administration During Out-of-Hospital Cardiac Arrest: A Randomized Trial. JAMA November 2009;302(20):2222-2229.

Ong ME et al. Survival outcomes with the introduction of intravenous epinephrine in the management of out-of-hospital cardiac arrest. Ann Emerg Med 2007;50(6):635-42.

Jacobs IG et al. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomized double-blind placebo-controlled trial. Resuscitation 2011;82:1138- 1143.

Context: Epinephrine is considered standard of care for cardiac arrest in kids and adults. Surprisingly, there are no randomized controlled clinical trials that show it is of benefit. We know from past studies that high-dose epinephrine got more patients to the hospital alive, but there was no increase in survival to hospital discharge. What about regular dose of epinephrine?  Is there any evidence for its use?

Abstract Thinking (PubMed)

Background: There is little evidence from clinical trials that the use of adrenaline (epinephrine) in treating cardiac arrest improves survival, despite adrenaline being considered standard of care for many decades.

The aim of our study was to determine the effect of adrenaline on patient survival to hospital discharge in out of hospital cardiac arrest.

Methods: We conducted a double blind randomised placebo-controlled trial of adrenaline in out-of-hospital cardiac arrest. Identical study vials containing either adrenaline 1:1000 or placebo (sodium chloride 0.9%) were prepared. Patients were randomly allocated to receive 1 ml aliquots of the trial drug according to current advanced life support guidelines. Outcomes assessed included survival to hospital discharge (primary outcome), pre-hospital return of spontaneous circulation (ROSC) and neurological outcome (Cerebral Performance Category Score - CPC).

Results: A total of 4103 cardiac arrests were screened during the study period of which 601 underwent randomisation. Documentation was available for a total of 534 patients: 262 in the placebo group and 272 in the adrenaline group. Groups were well matched for baseline characteristics including age, gender and receiving bystander CPR. ROSC occurred in 22 (8.4%) of patients receiving placebo and 64 (23.5%) who received adrenaline (OR = 3.4; 95% CI 2.0-5.6). Survival to hospital discharge occurred in 5 (1.9%) and 11 (4.0%) patients receiving placebo or adrenaline respectively (OR = 2.2; 95% CI 0.7-6.3). All but two patients (both in the adrenaline group) had a CPC score of 1-2.

Conclusion: Patients receiving adrenaline during cardiac arrest had no statistically significant improvement in the primary outcome of survival to hospital discharge although there was a significantly improved likelihood of achieving ROSC.

Comment and Critique: The study design and methodology were sound, and the study was carried out well. However, it has a few problems. It was single-center in western Australia; ambulance response times were a bit slow (mean of ten minutes); and they did not enroll >2200 patients per group as planned. So it is underpowered to detect the primary outcome, namely a 2% increase in survival to discharge (beyond the 5% baseline). They also failed to enroll 906 patients who were eligible, and there was no comment on whether or not the patients missed were significantly different than those enrolled, potentially producing selection bias. In 67 patients the randomization number was lost or not recorded. There is no comment on the use of therapeutic hypothermia while hospitalized. Can we assume neither group received this treatment? Overall, the study showed the superiority of epinephrine in producing ROSC and survival to hospital admission.  It showed a trend toward improved survival to discharge but was underpowered to detect a true difference.

Change in Practice: I think we need to keep epinephrine in our resuscitation protocols. More patients will have ROSC and make it to the hospital. The real question is whether more will make it home neurologically intact, and this study can't answer that.

Further Reading:

Olasveengen TM et al. Intravenous Drug Administration During Out-of-Hospital Cardiac Arrest: A Randomized Trial. JAMA November 2009;302(20):2222-2229.

Ong ME et al. Survival outcomes with the introduction of intravenous epinephrine in the management of out-of-hospital cardiac arrest. Ann Emerg Med 2007;50(6):635-42.

Williams DJ et al. Comparative Effectiveness of Antibiotic Treatment Strategies for Pediatric Skin and Soft-Tissue Infections. Pediatrics 2011;128:e479-e487.

Context: What is the best antibiotic to use when kids have skin and soft tissue infection (SSTI)? Community acquired methicillin resistant S. aureus (MRSA) is on the rise and is responsible for over 70% of staphylococcal infections in the U.S.  Where I work, most strains are still sensitive to trimethoprim-sulfamethoxazole (TMP-SMX) and clindamycin, but which one is better?  Do we need antibiotics at all? Would good old cephalexin still work?  That sets up this article.

Abstract Thinking (PubMed)

Objective: To compare the effectiveness of clindamycin, trimethoprim-sulfamethoxazole, and ?-lactams for the treatment of pediatric skin and soft-tissue infections (SSTIs).

Methods: A retrospective cohort of children 0 to 17 years of age who were enrolled in Tennessee Medicaid, experienced an incident SSTI between 2004 and 2007, and received treatment with clindamycin (reference), trimethoprim-sulfamethoxazole, or a ?-lactam was created. Outcomes included treatment failure and recurrence, defined as an SSTI within 14 days and between 15 and 365 days after the incident SSTI, respectively. Adjusted models stratified according to drainage status were used to estimate the risk of treatment failure and time to recurrence.

Results: Among the 6407 children who underwent drainage, there were 568 treatment failures (8.9%) and 994 recurrences (22.8%). The adjusted odds ratios for treatment failure were 1.92 (95% confidence interval [CI]: 1.49-2.47) for trimethoprim-sulfamethoxazole and 2.23 (95% CI: 1.71-2.90) for ?-lactams. The adjusted hazard ratios for recurrence were 1.26 (95% CI: 1.06-1.49) for trimethoprim-sulfamethoxazole and 1.42 (95% CI: 1.19-1.69) for ?-lactams. Among the 41 094 children without a drainage procedure, there were 2435 treatment failures (5.9%) and 5436 recurrences (18.2%). The adjusted odds ratios for treatment failure were 1.67 (95% CI: 1.44-1.95) for trimethoprim-sulfamethoxazole and 1.22 (95% CI: 1.06-1.41) for ?-lactams; the adjusted hazard ratios for recurrence were 1.30 (95% CI: 1.18-1.44) for trimethoprim-sulfamethoxazole and 1.08 (95% CI: 0.99-1.18) for ?-lactams.

Conclusions: Compared with clindamycin, use of trimethoprim-sulfamethoxazole or ?-lactams was associated with increased risks of treatment failure and recurrence. Associations were stronger for those with a drainage procedure.

Comment and Critique: In kids requiring drainage of an abscess, the odds of treatment failure was almost double if TMP-SMX or a beta-lactam was used as opposed to clindamycin.  Recurrent infection was also higher in those receiving TMP-SMX or a beta-lactam, though not quite as large an effect was seen.  SSTI not requiring a drainage procedure still showed increased treatment failure with TMP-SMX and beta-lactams.  But there was only an association with increased recurrence when these kids received TMP-SMX, not with beta-lactams.  Most SSTIs that did not require drainage were likely a mix of staphylococcal and streptococcal infections.  Clindamycin and beta-lactams are effective for strep, but TMP-SMX is not.  The kids that got mupirocin or another antibiotic were excluded, but in sensitivity analysis these patients fared no differently than the group studied.  This study is limited by the fact that it is a retrospective review of the Medicaid database and uses ICD-9 codes and CPT codes to determine the cohorts.  No doubt some patients were not included or potentially misclassified.  We can be reassured somewhat by a small validation cohort, in which 60 charts were pulled to see if their Medicaid record search reflected what really happened to the patients, and it did.

Change in Practice: If you have a child presenting with SSTI, choose clindamycin as your drug of choice for now.  TMP-SMX is not the best antibiotic in these patients.

Further Reading

Duong M et al. Randomized, controlled trial of antibiotics in the management of community acquired skin abscesses in the pediatric patient. Ann Emerg Med 2010;55(5):401-407.

Centers for Disease Control and Prevention. Methicillin-resistant Staphylococcus aureus (MRSA) infections. www.cdc.gov/mrsa.

Williams DJ et al. Comparative Effectiveness of Antibiotic Treatment Strategies for Pediatric Skin and Soft-Tissue Infections. Pediatrics 2011;128:e479-e487.

Context: What is the best antibiotic to use when kids have skin and soft tissue infection (SSTI)? Community acquired methicillin resistant S. aureus (MRSA) is on the rise and is responsible for over 70% of staphylococcal infections in the U.S.  Where I work, most strains are still sensitive to trimethoprim-sulfamethoxazole (TMP-SMX) and clindamycin, but which one is better?  Do we need antibiotics at all? Would good old cephalexin still work?  That sets up this article.

Abstract Thinking (PubMed)

Objective: To compare the effectiveness of clindamycin, trimethoprim-sulfamethoxazole, and ?-lactams for the treatment of pediatric skin and soft-tissue infections (SSTIs).

Methods: A retrospective cohort of children 0 to 17 years of age who were enrolled in Tennessee Medicaid, experienced an incident SSTI between 2004 and 2007, and received treatment with clindamycin (reference), trimethoprim-sulfamethoxazole, or a ?-lactam was created. Outcomes included treatment failure and recurrence, defined as an SSTI within 14 days and between 15 and 365 days after the incident SSTI, respectively. Adjusted models stratified according to drainage status were used to estimate the risk of treatment failure and time to recurrence.

Results: Among the 6407 children who underwent drainage, there were 568 treatment failures (8.9%) and 994 recurrences (22.8%). The adjusted odds ratios for treatment failure were 1.92 (95% confidence interval [CI]: 1.49-2.47) for trimethoprim-sulfamethoxazole and 2.23 (95% CI: 1.71-2.90) for ?-lactams. The adjusted hazard ratios for recurrence were 1.26 (95% CI: 1.06-1.49) for trimethoprim-sulfamethoxazole and 1.42 (95% CI: 1.19-1.69) for ?-lactams. Among the 41 094 children without a drainage procedure, there were 2435 treatment failures (5.9%) and 5436 recurrences (18.2%). The adjusted odds ratios for treatment failure were 1.67 (95% CI: 1.44-1.95) for trimethoprim-sulfamethoxazole and 1.22 (95% CI: 1.06-1.41) for ?-lactams; the adjusted hazard ratios for recurrence were 1.30 (95% CI: 1.18-1.44) for trimethoprim-sulfamethoxazole and 1.08 (95% CI: 0.99-1.18) for ?-lactams.

Conclusions: Compared with clindamycin, use of trimethoprim-sulfamethoxazole or ?-lactams was associated with increased risks of treatment failure and recurrence. Associations were stronger for those with a drainage procedure.

Comment and Critique: In kids requiring drainage of an abscess, the odds of treatment failure was almost double if TMP-SMX or a beta-lactam was used as opposed to clindamycin.  Recurrent infection was also higher in those receiving TMP-SMX or a beta-lactam, though not quite as large an effect was seen.  SSTI not requiring a drainage procedure still showed increased treatment failure with TMP-SMX and beta-lactams.  But there was only an association with increased recurrence when these kids received TMP-SMX, not with beta-lactams.  Most SSTIs that did not require drainage were likely a mix of staphylococcal and streptococcal infections.  Clindamycin and beta-lactams are effective for strep, but TMP-SMX is not.  The kids that got mupirocin or another antibiotic were excluded, but in sensitivity analysis these patients fared no differently than the group studied.  This study is limited by the fact that it is a retrospective review of the Medicaid database and uses ICD-9 codes and CPT codes to determine the cohorts.  No doubt some patients were not included or potentially misclassified.  We can be reassured somewhat by a small validation cohort, in which 60 charts were pulled to see if their Medicaid record search reflected what really happened to the patients, and it did.

Change in Practice: If you have a child presenting with SSTI, choose clindamycin as your drug of choice for now.  TMP-SMX is not the best antibiotic in these patients.

Further Reading

Duong M et al. Randomized, controlled trial of antibiotics in the management of community acquired skin abscesses in the pediatric patient. Ann Emerg Med 2010;55(5):401-407.

Centers for Disease Control and Prevention. Methicillin-resistant Staphylococcus aureus (MRSA) infections. www.cdc.gov/mrsa.

Dr. Creech is an expert on MRSA and was senior author for the "clindamycin beats TMP-SMX" study we just covered. Get the scoop on MRSA straight from the author.

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Dr. Creech is an expert on MRSA and was senior author for the "clindamycin beats TMP-SMX" study we just covered. Get the scoop on MRSA straight from the author.

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Is RSI safe in preemies? Many neonatologists just intubate without drugs. Shouldn't we do the same? Listen in to find out what to do the next time an ex-preemie shows up needing an airway.

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Is RSI safe in preemies? Many neonatologists just intubate without drugs. Shouldn't we do the same? Listen in to find out what to do the next time an ex-preemie shows up needing an airway.

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What's up! Vlad IA et al.  Patient perceptions of the potential lethality associated with deliberate self-poisoning. Emergency Medicine Australasia 2011;23:580-586.

Sum up! How do patient perceptions of how deadly their overdose was compare to toxicologists' risk assessment and a patient's suicidality?

This single-centre, prospective, observational study enrolled patients presenting with deliberate self-poisoning to a tertiary referral centre.  After patients were medically fit for discharge, they were interviewed by a member of the consult liaison psychiatry team.  After verbal consent, they were surveyed on their intention, planning, and suicidality, assessed according to the Pierce Suicide Intent Scale.  They graded their expectation of the overdose on a 10 cm visual analogue scale with 0 being harmless and 10 being certain to cause death.  Demographic data and details of the overdose were extracted on a preformatted tox sheet and was assessed by a panel of three toxicologist who rated the overdose's lethality by consensus on a 10 cm visual analogue scale with 0 being non-toxic, and 10 being universally lethal even with full medical intervention.

Of the 651 eligible patients, 202 (31%) patients were enrolled, 103 (51 %) stated it was their intention to kill themselves, and 44 (22%) had left suicide notes.  58% were female and median age was 33. The drugs used were what you'd expect with 15 to 20% in each of benzodiazepines, paracetamol (acetaminophen), antidepressants, antipsychotics, and 30% other. Odds of taking benzodiazepines increased significantly with increasing age, and odds of taking antipsychotics decreased with increasing age. The tablets were 70% prescription, 9% someone else's prescription, and 22% over the counter. 71% arrived by ambulance with 82% of ambulance called by family or friends. 51% stated they were trying to kill themselves, and 69% stated the self-poisoning was an impulsive act.  61% reported a previous self-poisoning, with the median time since the last self-poisoning being 7 days with (interquartile [IQR] range 0 to 365 days). The most common expectation of the overdose was sleep-inducing death. 78% had consumed alcohol with a median of 7 standard drinks, with a median blood alcohol level of 0.14mg/L.

Median patient VAS was 5.8 (IQR range of 2.3 to 8.3). Median toxicologist VAS was 1.4 (IQR range 0.6 to 2.8). Mismatch between toxicologist and patient assessment was arbitrarily defined as 1cm on the VAS, and not surprisingly, the difference between the two was highly statistically significant, p <0.0001. There was strong correlation between the Pierce Suicidal Intent Scale and patient VAS, toxicologist VAS, and it was the only independent predictor of correlation between patient and toxicologist VAS.

Hang up! This is a moderately sized study looking at an understudied area with clinically applicable results and some very useful epidemiological data.  They have used validated tools where they could, and made efforts to assess the reliability of the unvalidated tools when they could not.

Being single-centre, with only a 31% enrolment rate, may limit generalisability, but the epidemiology seems to match what I see in my ED.  Their initial assessment of the interrater reliability of the toxicologist VAS was poor, but improved with re-assessment.

Upshot! The epidemiological information is useful to know, and should leave you cautious about discharging patients post self-poisoning without psychiatry assessment and ironclad follow up with support services.  The high rate of representation and how soon afterwards (a quarter the same day, and half within the week) really gives pause for thought.

What's up! Vlad IA et al.  Patient perceptions of the potential lethality associated with deliberate self-poisoning. Emergency Medicine Australasia 2011;23:580-586.

Sum up! How do patient perceptions of how deadly their overdose was compare to toxicologists' risk assessment and a patient's suicidality?

This single-centre, prospective, observational study enrolled patients presenting with deliberate self-poisoning to a tertiary referral centre.  After patients were medically fit for discharge, they were interviewed by a member of the consult liaison psychiatry team.  After verbal consent, they were surveyed on their intention, planning, and suicidality, assessed according to the Pierce Suicide Intent Scale.  They graded their expectation of the overdose on a 10 cm visual analogue scale with 0 being harmless and 10 being certain to cause death.  Demographic data and details of the overdose were extracted on a preformatted tox sheet and was assessed by a panel of three toxicologist who rated the overdose's lethality by consensus on a 10 cm visual analogue scale with 0 being non-toxic, and 10 being universally lethal even with full medical intervention.

Of the 651 eligible patients, 202 (31%) patients were enrolled, 103 (51 %) stated it was their intention to kill themselves, and 44 (22%) had left suicide notes.  58% were female and median age was 33. The drugs used were what you'd expect with 15 to 20% in each of benzodiazepines, paracetamol (acetaminophen), antidepressants, antipsychotics, and 30% other. Odds of taking benzodiazepines increased significantly with increasing age, and odds of taking antipsychotics decreased with increasing age. The tablets were 70% prescription, 9% someone else's prescription, and 22% over the counter. 71% arrived by ambulance with 82% of ambulance called by family or friends. 51% stated they were trying to kill themselves, and 69% stated the self-poisoning was an impulsive act.  61% reported a previous self-poisoning, with the median time since the last self-poisoning being 7 days with (interquartile [IQR] range 0 to 365 days). The most common expectation of the overdose was sleep-inducing death. 78% had consumed alcohol with a median of 7 standard drinks, with a median blood alcohol level of 0.14mg/L.

Median patient VAS was 5.8 (IQR range of 2.3 to 8.3). Median toxicologist VAS was 1.4 (IQR range 0.6 to 2.8). Mismatch between toxicologist and patient assessment was arbitrarily defined as 1cm on the VAS, and not surprisingly, the difference between the two was highly statistically significant, p <0.0001. There was strong correlation between the Pierce Suicidal Intent Scale and patient VAS, toxicologist VAS, and it was the only independent predictor of correlation between patient and toxicologist VAS.

Hang up! This is a moderately sized study looking at an understudied area with clinically applicable results and some very useful epidemiological data.  They have used validated tools where they could, and made efforts to assess the reliability of the unvalidated tools when they could not.

Being single-centre, with only a 31% enrolment rate, may limit generalisability, but the epidemiology seems to match what I see in my ED.  Their initial assessment of the interrater reliability of the toxicologist VAS was poor, but improved with re-assessment.

Upshot! The epidemiological information is useful to know, and should leave you cautious about discharging patients post self-poisoning without psychiatry assessment and ironclad follow up with support services.  The high rate of representation and how soon afterwards (a quarter the same day, and half within the week) really gives pause for thought.

Isotonic fluid prevents renal failure in kids if given prior to HUS onset, but how can you know who is developing HUS vs just another gastroenteritis?  Find out in this week's podcast.

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What's up! Hickey CA et al. Early Volume Expansion During Diarrhea and Relative Nephroprotection During Subsequent Hemolytic Uremic Syndrome. Arch Pediatr Adolesc Med 2011;doi:10.1001/archpediatrics.2011.152.

Sum up! Is early volume expansion with saline associated with a lower risk of oligoanuria in kids with developing HUS?  In this prospective, multicenter, observational study, 50 children with hemolytic uremic syndrome (HUS) were followed to determine what variables were associated with oligoanuria (defined as urine output <0.5ml/kg/hr for at least one day after HUS onset) or nonoliguria.  They found that 21/25 (84%) children who received no IV fluid in the first four days of illness developed oligoanuria vs. only 13/25 (52%) children who received IV fluids.  The relative risk of oligoanuria was 1.6 (95% CI 1.1-2.4) for kids that did not receive any IV fluid in the first four days.  That means the number needed to treat (NNT) with IV fluid in the first four days of illness to prevent one case of oligoanuria was 3.  Volume of IV fluid infused over the first four days was the only variable that correlated with nonoliguria using logistic regression (OR 1.4, 95% CI 1.0-1.9).  None of the children in the study were hospitalized or intubated for acute pulmonary edema.

Hang-up! "The first four days of illness" was defined as the time between diarrhea onset and the time of HUS onset (i.e. microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency).  This is one of the problems with the study.  How do you know you are treating a kid with developing HUS vs. just another kid with diarrhea?  Bloody diarrhea, fever, greater severity of illness, and the presence of a local outbreak may provide clues!  86% of the kids in this study had bloody diarrhea, and nearly all of them had vomiting.

Upshot! Early isotonic IV fluid administration after the onset of diarrhea but prior to the development of HUS was associated with renal protection.  If you can catch patients early, give them saline for volume expansion to prevent oligoanuria in HUS.  Keep this in mind in kids with clinical features more suggestive of HUS (i.e. bloody stool, vomiting, ill appearing, febrile) especially if there is an outbreak of HUS in your area.

Isotonic fluid prevents renal failure in kids if given prior to HUS onset, but how can you know who is developing HUS vs just another gastroenteritis?  Find out in this week's podcast.

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What's up! Hickey CA et al. Early Volume Expansion During Diarrhea and Relative Nephroprotection During Subsequent Hemolytic Uremic Syndrome. Arch Pediatr Adolesc Med 2011;doi:10.1001/archpediatrics.2011.152.

Sum up! Is early volume expansion with saline associated with a lower risk of oligoanuria in kids with developing HUS?  In this prospective, multicenter, observational study, 50 children with hemolytic uremic syndrome (HUS) were followed to determine what variables were associated with oligoanuria (defined as urine output <0.5ml/kg/hr for at least one day after HUS onset) or nonoliguria.  They found that 21/25 (84%) children who received no IV fluid in the first four days of illness developed oligoanuria vs. only 13/25 (52%) children who received IV fluids.  The relative risk of oligoanuria was 1.6 (95% CI 1.1-2.4) for kids that did not receive any IV fluid in the first four days.  That means the number needed to treat (NNT) with IV fluid in the first four days of illness to prevent one case of oligoanuria was 3.  Volume of IV fluid infused over the first four days was the only variable that correlated with nonoliguria using logistic regression (OR 1.4, 95% CI 1.0-1.9).  None of the children in the study were hospitalized or intubated for acute pulmonary edema.

Hang-up! "The first four days of illness" was defined as the time between diarrhea onset and the time of HUS onset (i.e. microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency).  This is one of the problems with the study.  How do you know you are treating a kid with developing HUS vs. just another kid with diarrhea?  Bloody diarrhea, fever, greater severity of illness, and the presence of a local outbreak may provide clues!  86% of the kids in this study had bloody diarrhea, and nearly all of them had vomiting.

Upshot! Early isotonic IV fluid administration after the onset of diarrhea but prior to the development of HUS was associated with renal protection.  If you can catch patients early, give them saline for volume expansion to prevent oligoanuria in HUS.  Keep this in mind in kids with clinical features more suggestive of HUS (i.e. bloody stool, vomiting, ill appearing, febrile) especially if there is an outbreak of HUS in your area.

If referral hospitals import outside images, do patients get fewer repeat x-rays and CT scans? You bet!  This contains my little soap box as well.

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If referral hospitals import outside images, do patients get fewer repeat x-rays and CT scans? You bet!  This contains my little soap box as well.

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What is one hospital's experience with small kids (less than 20kg) treated with BiPAP for acute bronchospasm?  It appears safe, but possibly overused.

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What is one hospital's experience with small kids (less than 20kg) treated with BiPAP for acute bronchospasm?  It appears safe, but possibly overused.

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Is appendicitis better treated with cold steel and bright lights or antibiotics?

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Is appendicitis better treated with cold steel and bright lights or antibiotics?

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Five articles this week: 1) ED wait time matters. 2) CT is sensitive for appendicitis. 3) Broselow tape is better than physician weight estimate. 4) Nesiritide does no good and no harm. 5) Statins and succinylcholine don't increase muscle injury risk.

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Five articles this week: 1) ED wait time matters. 2) CT is sensitive for appendicitis. 3) Broselow tape is better than physician weight estimate. 4) Nesiritide does no good and no harm. 5) Statins and succinylcholine don't increase muscle injury risk.

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Which is better for sedating agitated patients, droperidol, midazolam, or both? Find out in this Australian article.

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Which is better for sedating agitated patients, droperidol, midazolam, or both? Find out in this Australian article.

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If we wait and observe kids with minor traumatic brain injury prior to making imaging decisions, will fewer kids have head CT scans ordered? Turns out, the answer is YES!

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If we wait and observe kids with minor traumatic brain injury prior to making imaging decisions, will fewer kids have head CT scans ordered? Turns out, the answer is YES!

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