2009年12月22日 星期二

小兒發燒:ACT好還是NSAIDs好?

Feverish debate
When you see a young child with a fever, what do you recommend that parents do? Give paracetamol alone, paracetamol and ibuprofen, or ibuprofen alone? This report of a high quality study of 156 children concludes that we should recommend ibuprofen alone.
  • Dual therapy (ibuprofen plus paracetamol) reduced fever better than paracetamol alone in the first 24 hours
  • But dual therapy was no better than ibuprofen alone in the first 24 hours
  • Ibuprofen alone was best at making the child feel better in the first 48 hours
However, a comment says that reduction of fever is of no value if the child does not feel better. Fever helps the body combat infection; antipyretics may prolong the duration of infection, without providing any reduction in fever seizures. So, "we should use ibuprofen if an antipyretic is needed (which is seldom) and not routinely combine paracetamol with ibuprofen."

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Source: Evidence-Bases Medicine 2009;14:174

2009年12月18日 星期五

院外ACLS不須IV給藥?

Do IV Meds Matter in Out-of-Hospital Cardiac Arrest?
Use of IV drugs did not affect long-term neurological outcome or survival.

Intravenous access and drug administration have long been central elements of advanced cardiac life support (ACLS) protocols despite the absence of evidence that they improve outcomes. In a randomized, controlled, nonblinded trial, 851 consecutive adult patients with out-of-hospital, nontraumatic cardiac arrest in Oslo, Norway from 2003 to 2008 were randomized to receive ACLS with IV access and drug administration (epinephrine, atropine, and amiodarone were used) or ACLS with no IV access.

In the group that received ACLS with no IV access, IV access was established within 5 minutes after return of spontaneous circulation (ROSC). In both groups, patients with ventricular fibrillation received cardiopulmonary resuscitation for 3 minutes before the first shock and between unsuccessful series of shocks. Endotracheal intubation was standard, and postresuscitation therapeutic hypothermia was instituted regardless of initial rhythm or course of arrest. Quality of CPR was determined by transthoracic impedance signals from defibrillators. The primary outcome was survival to discharge.

The rate of hospital admission for patients with ROSC was significantly higher in the group with IV access than in the group without IV access (32% vs. 21%). However, no significant differences were found between the IV-access and no-IV-access groups in rates of survival to discharge (10% and 9%), survival with favorable neurological outcome (10% and 8%), and survival at 1 year (10% and 8%). CPR was performed according to guidelines, and its quality was similar in both groups.

Comment:
This first effort to evaluate the effect of IV access and drug administration on outcomes in patients with out-of-hospital cardiac arrest, after more than 4 decades of use, yields provocative results: These long-standing interventions were not associated with improvement in long-term survival or neurological outcome. The results are in concert with those from studies in which epinephrine, atropine, and amiodarone improved short-term but not long-term outcomes compared with placebo. In addition, IV access had no negative effect on the quality of CPR. This trial begs for research targeted at novel pharmacologic therapies and should prompt the rethinking of ACLS guidelines.


John A. Marx, MD, FAAEM
Published in Journal Watch Emergency Medicine December 18, 2009
Citation(s): Olasveengen TM et al. Intravenous drug administration during out-of-hospital cardiac arrest: A randomized trial. JAMA 2009 Nov 25; 302:2222.

2009年12月9日 星期三

Emergency obstetric care


Decision-making algorithm in emergency obstetric care.
C-section, cesarean section;
FHTs, fetal heart tones;
US, ultrasonography.

2009年12月8日 星期二

Transtubular potassium gradient (TTKG)


Indications:Hyperkalemia

Precautions:
  • Results altered by Hyperkalemia Management.
  • Obtain lab sample prior to intervention if possible.
  • Do not delay treatment in emergent Hyperkalemia.
Labs:
  • Serum Potassium and Serum Osmolality.
  • Spot urine for Urine Potassium and Urine Osmolality.
Formula of Transtubular Potassium Gradient (TTPG):
  • TTPG = (Urine K+ x Serum Osm)/(Serum K+ x Urine Osm)
    ... where K+ is potassium and Osm is Osmolality.
Interpretation of Fractional Excretion of Potassium:
  • TTPG <6-8%:>
  • TTPG). TTPG >6-8: Extrarenal cause of Hyperkalemia (May also be increased in Chronic Renal Failure).

【新藥】Dabigatran有可能取代warfarin?!

Oral Alternative to Warfarin for Venous Thromboembolism?
Dabigatran was safe and effective and had advantages over warfarin.

Dabigatran is a direct oral thrombin inhibitor that, unlike warfarin, can be given in a fixed dose and requires no laboratory monitoring. In a recently published study, dabigatran compared favorably with warfarin in patients with atrial fibrillation (JW Cardiol Sep 1 2009).
In this new industry-sponsored double-blind trial, more than 2500 patients with acute venous thromboembolism (69% with deep venous thrombosis [DVT] only, 21% with pulmonary embolism only, and 10% with both) were randomized to receive either warfarin or dabigatran after initial heparin therapy. At 6 months, significant differences were found between the dabigatran and warfarin groups in incidence of recurrent venous thromboembolism (2.4% and 2.1%) or major bleeding (1.6% and 1.9%). A combined endpoint of major bleeding plus clinically relevant nonmajor bleeding occurred less often with dabigatran (5.6% vs. 8.8%). One side effect, dyspepsia, occurred more commonly with dabigatran than with warfarin (3.1% vs. 0.7%).

Comment:
Dabigatran, which is not yet FDA approved, appears to be comparable to warfarin in both efficacy and safety in patients with venous thromboembolism. Its advantage, compared with warfarin, is that it requires neither laboratory monitoring nor dose adjustments. A previous direct oral thrombin inhibitor, ximelagatran, was effective but failed to gain FDA approval because of hepatotoxicity; in contrast, no hepatotoxicity has occurred in studies of dabigatran. Note that both dabigatran and an oral direct inhibitor of factor Xa (rivaroxaban) already have been approved for use in Canada and some European countries for DVT prophylaxis following total hip or knee arthroplasty but not yet for atrial fibrillation or DVT treatment.


Allan S. Brett, MD
Published in Journal Watch General Medicine December 8, 2009
Citation(s): Schulman S et al. Dabigatran versus warfarin in the treatment of acute venous thromboembolism. N Engl J Med 2009 Dec 10; 361:2342.

2009年11月24日 星期二

肥鵝肝醬

Foie gras
This editorial and study point out that:
  • Non-alcoholic fatty liver disease (NAFLD) is the most common form of chronic liver disease in both children and adults
  • It is likely to become a serious public health problem worldwide
  • It is closely associated with obesity and insulin resistance
  • It includes a spectrum of diseases from simple fatty liver (steatosis) to fibrosis and cirrhosis
  • This study shows it can take only 10-20 years for the disease to progress from its first signs to irreversible end-stage disease
  • There is no effective drug treatment - early diagnosis and lifestyle changes are key to stop disease progression
  • Disease markers need to be developed to identify those most at risk.
---
Source: Gut 2009;58:1442

Migraine with aura and stroke

Is everyone who gets migraines at an increased risk of a stroke?
This large survey and editorial say:
  • Only the quarter of migraine sufferers who get an aura are at increased risk of stroke
  • Migraine with aura doubles a person's risk of having a stroke
  • Migraine is also associated with an increased risk of transient ischaemic attacks and angina. It isn't clear whether this is true for all migraine sufferers or only those with aura
  • Migraine without aura isn't associated with an increased risk of stroke
  • Aura is a transient neurological disturbance before or during the headache
  • Sensitivity to light, visual blurring, and fatigue are common accompaniments to migraine but should not be confused with aura
  • People who have migraine with aura should have their other risk factors treated (smoking, blood pressure, cholesterol, and blood glucose)
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Source: BMJ 2009;339:b4380

2009年11月20日 星期五

解決急診爆滿床:於病房走廊加床是安全的對策

Is It Safe to Admit Boarder Patients to Inpatient Hallways?
A study at a single academic ED shows that the practice is safe.

Caring for emergency department patients in hallways has become the norm as hospital crowding has become pervasive. One approach to reducing ED crowding during times of high ED and inpatient census is to augment inpatient capacity by admitting selected ED boarder patients to hallways on inpatient floors, instead of boarding them in the ED. This approach essentially "shares the pain" of hospital crowding.

In a retrospective cohort study, investigators compared outcomes for patients who were admitted to inpatient hallways with outcomes for patients who were admitted to standard inpatient beds at a single U.S. academic ED between 2004 and 2008. Patients who did not require intensive care unit (ICU) or step-down care or high-intensity nursing care for such needs as continuous suction, high-flow O2, or seizure monitoring were eligible to board in inpatient hallways.

Of 55,062 ED patients who were admitted during the study period, 4% were admitted to an inpatient hallway. ED census at time of triage was significantly higher for patients admitted to hallways compared with patients admitted to standard beds, and time from ED triage to admission was significantly longer for patients admitted to hallways. Approximately 25% of patients admitted to hallways were assigned to a standard bed immediately on arrival to the inpatient unit, 25% were placed in a room within 1 hour, and the remaining 50% waited approximately 8 hours for a room. Patients admitted to hallways, compared with those admitted to standard beds, had significantly lower rates of in-hospital mortality (1.1% vs. 2.6%) and transfer to an ICU (2.5% vs. 6.7%).

Comment:
Although inpatients in other countries are commonly boarded in inpatient hallways, this practice has met significant resistance in the U.S., with risk to patient safety cited as the major concern. At this study's single institution, boarding selected patients on inpatient units was not associated with risk to patient safety. Other institutions should consider implementing inpatient-unit boarding as part of a multifaceted approach to crowding.


Richard D. Zane, MD, FAAEM
Published in Journal Watch Emergency Medicine November 20, 2009
Citation(s): Viccellio A et al. The association between transfer of emergency department boarders to inpatient hallways and mortality: A 4-year experience. Ann Emerg Med 2009 Oct; 54:487.

2009年11月12日 星期四

【NEJM】H1N1 重症病人的特徵

What are patient risk factors for a requirement of intensive care services in H1N1 influenza?
In the ANZIC study, infants (0 to 1 year of age), pregnant women, and adults 25 to 64 years of age appeared to be at particular risk for severe disease. Indigenous groups were overrepresented among patients who were admitted to ICUs: 10% in Australia and 25% in New Zealand. Further, both the ANZIC study and other studies indicate that obesity is a likely risk factor for increased severity of H1N1. In the ANZIC study, 29% of patients had a body-mass index (the weight in kilograms divided by the square of the height in meters) of 35 or more.

What is the risk of death after infection with the H1N1 influenza virus as compared to the risk of death after infection with seasonal influenza?
The proportion of patients who died in the ANZIC study (14%) is no higher than that previously reported among patients with seasonal influenza A who were admitted to an ICU. Patients admitted to an ICU with seasonal influenza A predominantly are elderly and have coexisting conditions. In H1N1, although older age, the presence of coexisting conditions, and a requirement for invasive ventilation were independently associated with increased risk of death in the ANZIC study, the majority of deaths occurred in younger patients because there were greater numbers of younger patients in the study cohort.

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New England Journal of Medicine - Vol. 361, No. 20, November 12, 2009

2009年11月6日 星期五

推動OHCA 低溫治療:是時候了...

Induced Hypothermia After VF Cardiac Arrest Improves Outcomes
Hypothermia led to significantly better survival rates and neurological outcomes in patients with ventricular fibrillation but not in those with other initial rhythms.

Despite evidence that induced hypothermia therapy after cardiac arrest improves neurological outcomes and survival, cooling protocols have not been widely implemented. In a retrospective observational study, researchers compared outcomes in consecutive patients with out-of-hospital cardiac arrest who were resuscitated in the 2 years before (204 patients) and the 2 years after (287) implementation of a therapeutic hypothermia protocol at a teaching hospital in Seattle. Patients with severe infection, active bleeding, or nonintact skin from recent burns or who were in a persistent vegetative state prior to cardiac arrest were excluded.
Patients in the hypothermia group were cooled with ice packs, cooling blankets, or cooling pads and received intravenous vecuronium and diazepam. Temperature was measured with an esophageal probe; the goal of 32°C–34°C was achieved in 65% of patients. Passive rewarming commenced after 24 hours of cooling.

Rates of survival to hospital discharge were significantly higher in the hypothermia group than in the control group among patients with an initial rhythm of ventricular fibrillation (VF) (54% vs. 39%) but did not differ among patients with other rhythms. Similarly, the rate of favorable neurological outcomes was significantly higher in the hypothermia group than in the control group among patients with VF (35% vs. 15%).

Comment: Although a greater incidence of witnessed arrests in the hypothermia group (66%) than in the control group (57%) might have skewed the results, the findings suggest that cardiac arrest patients with an initial rhythm of VF might benefit from therapeutic cooling. Based on this and previous outcome studies (JW Emerg Med Oct 27 2006) and on other studies showing that induced hypothermia in the emergency department is feasible (JW Emerg Med Jul 11 2008), it is time for EDs (and some emergency medical services systems) to implement hypothermia protocols for comatose survivors of cardiac arrest.


Kristi L. Koenig, MD, FACEP
Published in Journal Watch Emergency Medicine November 6, 2009

Citation(s): Don CW et al. Active surface cooling protocol to induce mild therapeutic hypothermia after out-of-hospital cardiac arrest: A retrospective before-and-after comparison in a single hospital. Crit Care Med 2009 Sep 16; [e-pub ahead of print]. (http://tinyurl.com/yht8qs7)

2009年11月2日 星期一

急診放射影像十戒

急診放射影像十戒
【1】先問 Hx 做 PE 再照片子
【2】處置要針對病人而非針對片子
【3】沒看過病人就不要對片子下最後結論
【4】讀片要讀好片:注意明暗、解析度、大小
【5】片子要全看,不要只看部份,不要跳著看
【6】讀片有疑惑時,先重新評估病人
【7】記得〝rule of 2〞:2角度、2關節、2側、2張、2次
【8】做完 procedure 後再照一張
【9】不確定就發問
【10】建立失效安全把關機制

2009年10月29日 星期四

TPA for stroke 可延長至 4.5 小時

Stroke treatment with alteplase given 3.0-4.5 h after onset of acute ischaemic stroke (ECASS III).

Conclusion:
Our results support the use of alteplase up to 4.5 h after the onset of stroke symptoms across a broad range of subgroups of patients who meet the requirements of the European product label but miss the approved treatment window of 0-3 h.

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Lancet Neurol. 2009 Oct 20.
http://linkinghub.elsevier.com/retrieve/pii/S1474-4422(09)70264-9

HIV risk of percutaneous inoculation

What is the risk of HIV transmission after percutaneous inoculation?
The overall rate of HIV transmission through percutaneous inoculation (i.e., by means of a needle or other instrument that pierces the skin) is widely reported to be 0.3% (95% confidence interval [CI], 0.2 to 0.5); features of exposure that are associated with a higher rate of transmission include a needle that was used to cannulate a blood vessel in the source patient, advanced HIV disease in the source patient, a deep needlestick, and visible blood on the surface of the instrument. Theoretically, any exposure that involves piercing of the skin may transmit infection, but clinical judgment is required to assess the likelihood that the inoculum is sufficient to pose a credible threat of transmission; many clinicians use a puncture that draws blood as a general threshold. Splashes of infectious material to mucous membranes (e.g., conjunctivae or oral mucosa) or broken skin also may transmit HIV infection (estimated risk per exposure, 0.09% [95% CI, 0.006 to 0.5]).

HIV risk of sexual exposure

What is the risk of HIV transmission after sexual exposure?
The per-contact risk of HIV transmission from sexual exposure varies according to the nature of the exposure. The estimated risks are 1 to 30% with receptive anal intercourse, 0.1 to 10.0% with insertive anal intercourse and receptive vaginal intercourse, and 0.1 to 1.0% with insertive vaginal intercourse. As compared with other forms of intercourse, oral intercourse is considered to pose a lower risk of HIV transmission, although good risk estimates are lacking. The risks of sexual transmission are difficult to quantify; the wide ranges reported for the risks of per-contact transmission derive from observational studies and are influenced by many factors, including the presence or absence of concomitant genital ulcer disease, other disease states, and cervical or anal dysplasia; circumcision status; the viral load in the genital compartment; and the degree of viral virulence.

2009年10月26日 星期一

誰說OHCA低溫治療一定要買昂貴儀器?

Cold saline infusion and ice packs alone are effective in inducing and maintaining therapeutic hypothermia after cardiac arrest

Aim of the study
Hypothermia treatment with cold intravenous infusion and ice packs after cardiac arrest has been described and used in clinical practice. We hypothesised that with this method a target temperature of 32–34°C could be achieved and maintained during treatment and that rewarming could be controlled.

Materials and methods
Thirty-eight patients treated with hypothermia after cardiac arrest were included in this prospective observational study. The patients were cooled with 4°C intravenous saline infusion combined with ice packs applied in the groins, axillae, and along the neck. Hypothermia treatment was maintained for 26h after cardiac arrest. It was estimated that passive rewarming would occur over a period of 8h. Body temperature was monitored continuously and recorded every 15min up to 44h after cardiac arrest.

Results
All patients reached the target temperature interval of 32–34°C within 279±185min from cardiac arrest and 216±177min from induction of cooling. In nine patients the temperature dropped to below 32°C during a period of 15min up to 2.5h, with the lowest (nadir) temperature of 31.3°C in one of the patients. The target temperature was maintained by periodically applying ice packs on the patients. Passive rewarming started 26h after cardiac arrest and continued for 8±3h. Rebound hyperthermia (>38°C) occurred in eight patients 44h after cardiac arrest.

Conclusions
Intravenous cold saline infusion combined with ice packs is effective in inducing and maintaining therapeutic hypothermia, with good temperature control even during rewarming.

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Resuscitation - 23 October 2009
(10.1016/j.resuscitation.2009.09.012)

2009年10月24日 星期六

【新知】Cardiocerebral Resuscitation

Researchers at the University of Arizona created a new protocol for the management of OHCA that they termed "cardiocerebral resuscitation." CCR consists of 3 major parts: (1) continuous chest compressions with no early ventilations preshock and postshock; (2) delayed intubation; and (3) early use of epinephrine. A recent study that compared CCR with standard CPR in patients with shockable rhythms demonstrated that both survival (47.2% vs 19.6%) and percentage of survivors with good neurologic outcome (83.3% vs 77.8%) were significantly improved in those who underwent CCR.

http://www.medscape.com/viewarticle/707616


Summary

Ewy and Kern, both leaders in the field of cardiac resuscitation, reviewed CCR and described ideal postresuscitation care. The "3 pillars" of CCR were described:

A. Compression-only CPR by anyone who witnessed the event.
B. CCR by emergency medical service personnel, assumed to be arriving > 5 minutes postarrest.
  1. 200 chest compressions (at 100/minute), delay intubation; second person to apply defibrillation pads and initiate passive oxygen insufflation (eg, 100% oxygen via facemask)
  2. Single shock if indicated, immediately followed by 200 more chest compressions (no pulse check after shock)
  3. Check for pulse and rhythm; note that this pulse check occurs 4 minutes after the CCR has begun
  4. EPI intravenously or intraosseously as soon as possible to improve central circulation, coronary circulation, and diastolic blood pressure
  5. Repeat (2) and (3) 3 times; intubate if no return of spontaneous circulation after 3 cycles; note that neither bag-valve-mask ventilation nor intubation occurs until 12 minutes after the CCR has begun
  6. Continue resuscitation efforts with minimal interruptions of chest compressions until resuscitation is successful or the person is pronounced dead
Viewpoint

In summary, the traditional mantra in emergency medicine of "A-B-C" has been turned upside-down by CCR. Aggressive management of the airway in those who have cardiac arrest is being relegated to a far lower priority. Good chest compressions and early EPI administration are the most important interventions when ventricular fibrillation is present in the circulation phase of cardiac arrest. Future studies will need to evaluate whether these concepts are applicable to nonshockable rhythms as well, although intuitively this seems reasonable. Finally, those who survive cardiac arrest should be treated with induced hypothermia, and pending more studies, they may benefit from early coronary angiography and PCI as well.

2009年10月23日 星期五

新版的「用力壓、快快壓」果然有效!

Compress the Chest: Better CPR Improves Survival from Out-of-Hospital Cardiac Arrest
Implementation of the 2005 AHA CPR guidelines that focus on uninterrupted chest compressions nearly doubled the odds of survival among patients with out-of-hospital cardiac arrest.

In 2005, the American Heart Association (AHA) released updated evidence-based guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, but does adherence to the revised protocol improve outcomes? Investigators compared rates of survival from out-of-hospital cardiac arrest among 606 adult patients treated before and 1021 treated after implementation of the 2005 AHA guidelines in a single large emergency medical services system.

Review of a convenience sample of 69 electronic electrocardiogram recordings showed significant improvement in CPR quality after guideline implementation, including improvements in mean chest-compression rate, proportion of time that patients received chest compressions, and median preshock and postshock pause times for compressions. Unadjusted rates of survival to hospital discharge were significantly higher after implementation of the guidelines than before (9.4% vs. 6.1%). Among patients with witnessed arrest whose initial rhythm was ventricular fibrillation on EMS arrival, survival rates improved significantly from 24% (19 of 78) before implementation to 30% (34 of 112) after. Multivariate regression analysis that adjusted for initial rhythm, sex, arrest location, and witnessed arrest showed 1.8 greater odds of survival in the postintervention period.

Comment: The promising results of this large study suggest the AHA was on the right track with its renewed focus on basic CPR, including the importance of providing uninterrupted chest compressions.


Kristi L. Koenig, MD, FACEP
Published in Journal Watch Emergency Medicine October 23, 2009

Citation(s): Sayre MR et al. Impact of the 2005 American Heart Association cardiopulmonary resuscitation and emergency cardiovascular care guidelines on out-of-hospital cardiac arrest survival. Prehosp Emerg Care 2009 Oct-Dec; 13:469.

AMI 之症狀表現:性別差異

Symptoms of a first acute myocardial infarction in women and men

Background: Many studies have compared women and men for symptoms of acute myocardial infarction (AMI), but findings have been inconsistent, largely because of varying inclusion criteria, different study populations, and different methods.

Objective: The purpose of this study was to analyze gender differences in symptoms in a well-defined, population-based sample of women and men who experienced a first AMI.

Methods: Information on symptoms was collected from the medical charts of all patients with a first AMI, aged 25 to 74 years, who had taken part in the INTERGENE (Interplay Between Genetic Susceptibility and Environmental Factors for the Risk of Chronic Diseases) study. INTERGENE was a population-based research program on risk factors for cardiovascular disease. Medical charts were reviewed for each patient to determine the symptoms of AMI, and the prevalence of each symptom was compared according to sex.

Results: The study included 225 patients with a first AMI: 52 women and 173 men. Chest pain was the most common symptom, affecting 88.5% (46/52) of the women and 94.8% (164/173) of the men, with no statistically significant difference between the sexes. Women had significantly higher rates of 4 symptoms: nausea (53.8% [28/52] vs 29.5% [51/173]; age-adjusted odds ratio [OR] = 2.78; 95% CI, 1.47–5.25), back pain (42.3% [22/52] vs 14.5% [25/173]; OR = 4.29; 95% CI, 2.14–8.62), dizziness (17.3% [9/52] vs 7.5% [13/173]; OR = 2.60; 95% CI, 1.04–6.50), and palpitations (11.5% [6/52] vs 2.9% [5/173]; OR = 3.99; 95% CI, 1.15–13.84). No significant gender differences were found in the proportions of patients experiencing arm or shoulder pain, diaphoresis, dyspnea, fatigue, neck pain, abdominal pain, vomiting, jaw pain, or syncope/lightheadedness. No significant differences were found in the duration, type, or location of chest pain. The medical charts listed numerically more symptoms in women than in men; 73.1% (38/52) of the women but only 48.0% (83/173) of the men reported >3 symptoms (age-adjusted OR = 3.26; 95% CI, 1.62–6.54).

Conclusions: Chest pain is the most common presenting symptom in both women and men with AMI. Nausea, back pain, dizziness, and palpitations were significantly more common in women. Women as a group displayed a greater number of symptoms than did men.

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Gender Medicine. Volume 6, Issue 3, September 2009, Pages 454-462
http://dx.doi.org/10.1016/j.genm.2009.09.007

類固醇治偏頭痛無效

Steroids for migraine headaches: a randomized double-blind, two-armed, placebo-controlled trial

Background:
Recurrence of migraine headache after treatment in the emergency department (ED) is common. Conflicting evidence exists regarding the utility of steroids in preventing migraine headache recurrence at 24–48 h.

Objective:
To determine if steroids decrease the headache recurrence in patients treated for migraine headaches in the ED.

Methods:
Double-blind placebo-controlled, two-tailed randomized trial. Patients aged >17 years with a moderately severe migraine headache diagnosed by treating Emergency Physician were approached for participation. Enrollees received either dexamethasone (10 mg i.v.) if intravenous access was utilized or prednisone (40 mg by mouth × 2 days) if no intravenous access was obtained. Each medication was matched with an identical-appearing placebo. Patients were contacted 24–72 h after the ED visit to assess headache recurrence.

Results:
A total of 181 patients were enrolled. Eight were lost to follow-up, 6 in the dexamethasone group and 2 in the prednisone arm. Participants had a mean age of 37 years (±10 years), with 86% female. Eighty-six percent met the International Headache Society Criteria for migraine headache. Of the 173 patients with completed follow-up, 20/91 (22%) (95% confidence interval [CI] 13.5–30.5) in the steroid arm and 26/82 (32%) (95% CI 21.9–42.1) in the placebo arm had recurrent headaches (p = 0.21).

Conclusion:
We did not find a statistically significant decrease in headache recurrence in patients treated with steroids for migraine headaches.

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http://www.jem-journal.com/article/PIIS0736467909007471/abstract

2009年10月22日 星期四

Management of Necrotizing Fasciitis

There are four general principles that guide the management of a necrotizing soft-tissue infection: (1) early identification, (2) source control, (3) antibiotics, and (4) supportive care. Early identification of a serious necrotizing soft-tissue infection may not be straightforward. The typical signs are erythema, purplish discoloration of the skin with bullae, edema, crepitus, and pain that seems disproportionate to the findings on examination. Since in many cases, not all these signs are present, practitioners may underestimate the extent of the disease process. Surgical control of the source of the infection is a lifesaving maneuver. Because of this, emphasis is placed on removing affected tissue, regardless of possible resultant cosmetic defects. Removal of the necrotic tissue and the bacterial load allows antibiotics to control the spread of bacteria more effectively. Because of the rapidity with which necrotizing fasciitis spreads, time is of the essence when dealing with source control. Despite early aggressive surgical débridement, mortality rates range from 16 to 45%.

New England Journal of Medicine - Vol. 361, No. 17, October 22, 2009

Epidemiology of Necrotizing Fasciitis

Necrotizing soft-tissue infections can be divided into two types: type I (polymicrobial) and type II (monomicrobial). Approximately 70% of infections are type I; type II infections usually involve group A streptococci. The incidence of necrotizing fasciitis is difficult to determine, since the classification and coding of these infections is poor; a conservative estimate is 1500 severe cases per year in the United States.

Risk factors for the development of these infections include diabetes, renal failure, liver failure, advanced age, behavior risks (e.g., intravenous drug abuse), and obesity. However, more than 20% of cases have no known risk factors. The patient in the case had recently given birth by means of a surgical procedure, and the wound could have been contaminated by organisms from the patient's skin or from a health care worker.

New England Journal of Medicine - Vol. 361, No. 17, October 22, 2009

2009年10月15日 星期四

Bacterial Diarrhea

Diagnosis of Bacterial Diarrhea
Most bacterial and nonbacterial enteropathogens produce nonspecific acute watery diarrhea. The rate of underreporting of cases of acute watery diarrhea that are caused by detectable enteric pathogens, including most cases of diarrhea caused by bacteria such as salmonella and campylobacter is substantial. Indications for stool culture include the presence of severe diarrhea (passage of six or more unformed stools per day), diarrhea of any severity that persists for longer than a week, fever, and multiple cases of illness that suggest an outbreak. Dysentery, with passage of blood and mucus in stools, suggests possible bacterial colitis, and stool samples are recommended. Stool cultures are not routinely recommended in most cases of watery diarrhea or traveler's diarrhea because of a low yield of bacterial pathogens.

Recommended treatment for bacterial diarrhea
For all cases of diarrhea, attention to fluid and electrolyte replacement is fundamental. Available data in children with acute diarrhea do support the continuation of oral feeding during the illness. Antimotility drugs such as loperamide and diphenoxylate hydrochloride, can reduce the number of stools passed and may be useful in controlling the stool rate with watery diarrhea. They should not be used without concomitant antibacterial therapy in patients with fever or dysentery in whom the drug may lead to increased contact time of the enteropathogen with the gut mucosa. Therapy with antimicrobial agents is important in most cases of diarrhea caused by invasive or inflammatory bacterial pathogens and is useful in other noninvasive forms of bacterial diarrhea.

Food poisoning

What characterizes the term “food poisoning”?

Food poisoning is the term used when a preformed toxin in food is ingested, resulting in intoxication rather than an enteric infection. Staphylococcus aureus causes vomiting within 2 to 7 hours after the ingestion of improperly cooked or stored food containing a heat-stable preformed toxin. Clostridium perfringens causes watery diarrhea without vomiting within 8 to 14 hours after the ingestion of contaminated meat, vegetables, or poultry. Strains of Bacillus cereus from contaminated fried rice, vegetable sprouts, or other food items produce one of two toxins that may result in disease resembling that caused by S. aureus or C. perfringens, depending on the toxin produced. Most cases of food poisoning are of short duration, with recovery occurring in 1 to 2 days. Although it is possible to confirm the cause of food poisoning by microbiologic methods, these are rarely used, and the diagnosis is made in nearly all cases clinically without laboratory confirmation.

New England Journal of Medicine - Vol. 361, No. 16, October 15, 2009

2009年10月8日 星期四

Top 10 Mistakes Made in Clinical Rotations

Top 10 Mistakes Made in Clinical Rotations
Kendra Campbell, Medical Student, Emergency Medicine, 10:38AM Oct 4, 2009

Last week, I watched a med student argue for 20 minutes with a patient about whether or not they were ambulating enough. His actions inspired me to make a top 10 list of mistakes that I've seen students make during their clinical rotations:

1. Arguing with a patient.
This is an exercise in futility, and is very unprofessional.

2. Reporting a physical finding without actually observing it.
I've even seen a student get in trouble for documenting a physical finding on a patient who had been discharged already.

3. Pimping your resident or attending.
Med school is similar to the military when it comes to respecting your place in the chain of command. Attendings pimp residents and med students. Residents pimp med students. Thou shalt not pimp up the chain.

4. Disrespecting the nurses.
Seriously, this is a huge no-no. If you want to make your life miserable, make the nurses hate you. If you want to enjoy your time at the hospital, befriend every nurse you meet.

5. Dressing inappropriately.
I've seen this rule broken many times, and yet it never fails to shock me. We've probably all seen at least one female wearing 4-inch stiletto heels, or showing so much cleavage that you could use their chest to make an anatomical drawing. There's a time and a place for everything, and the hospital is not a place to dress provocatively.

6. Documenting an important positive finding without alerting your resident or attending.
If you discover that a patient has rebound tenderness, or a temperature of 103.7, don't write this in a note and walk away. You must always alert your higher-ups to significant findings, or else you will find yourself getting chewed out for a good while.

7. Showing up late.
This is a particular pet peeve of mine, and one that some students seem to think is insignificant. People notice when you're late. It's unprofessional and disrespectful to the rest of the group. Traffic is not an excuse. Leave your residence early enough to get to the hospital with plenty of time to spare.

8. Performing a procedure without having been authorized to do so.
If the resident walks in on you placing a central line on a patient without their authorization, you will find yourself in deep trouble with the doctor, hospital, and potentially a courtroom.

9. Forgetting you are in a hospital.
This is something that is easier said than done. We spend so many hours in the hospital that it's easy to forget that we are surrounded by very ill people. It's not a high school football game; it's a hospital, people.

10. Being a slacker.
We all have seen students who try to get by with the bare minimum in everything they do. If you want to throw away a ridiculous amount of money, not learn anything, and end up being a crappy doctor, then by all means slack off during your clinical years. If you want to learn a lot and become an incredible doctor, then put in the time and effort.

2009年10月7日 星期三

何謂 DCS?

What is meant by “damage-control surgery”?

If a patient had hypothermia, acidosis, and diffuse bleeding during the first laparotomy, the surgical team will opt for a damage-control strategy. The term “damage control” originated in the U.S. Navy and referred to the ability of a ship to absorb damage while continuing to perform its mission. Damage-control laparotomy is widely practiced today in severely injured patients with trauma. The basic concept is to perform an abbreviated operation, focusing on controlling hemorrhage and contamination. This initial operation is followed by a period of resuscitation in the intensive care unit (ICU) to reverse the lethal triad of acidosis, hypothermia, and coagulopathy. The patients are taken back to the operating room for a definitive operation once the physiological disturbances have been corrected. Although used primarily for severely injured patients, this approach is equally useful for other critically ill patients who need an operation.

New England Journal of Medicine - Vol. 361, No. 15, October 8, 2009

外傷病患的死亡三角關係

What is the “lethal triad” in trauma patients?

The ominous trio of signs in trauma patients, including coagulopathy, acidosis, and hypothermia has been called the “lethal triad.” These factors perpetuate one another, thus creating a vicious cycle that is difficult to interrupt. Early development of coagulopathy is a well-recognized marker of the severity of an injury, and its presence is associated with a significantly increased risk of death.

New England Journal of Medicine - Vol. 361, No. 15, October 8, 2009

2009年9月22日 星期二

Oseltamivir Resistance and Antiviral Use

H1N1 Update: Oseltamivir Resistance and Antiviral Use

The CDC reports oseltamivir-resistant 2009 pandemic influenza A (H1N1) virus infection in two children who received prophylaxis and provides revised recommendations for antiviral use during the 2009 flu season.

Although sporadic cases of oseltamivir-resistant 2009 pandemic influenza A (H1N1) virus infection have been reported, oseltamivir remains an important tool in our armamentarium against flu. In July 2009, two girls residing in the same camp cabin in North Carolina developed oseltamivir-resistant 2009 (H1N1) virus infection while receiving oseltamivir as part of a mass prophylaxis program during an influenza outbreak. Both girls recovered fully. Whether the one girl case transmitted the virus to the other or whether both girls were infected by another camper is uncertain. One girl continued to receive prophylactic (not therapeutic) doses of oseltamivir during the first 4 days of her illness, which could have contributed to the development of resistance.

On September 8, 2009, the CDC updated recommendations for use of antiviral medications in the treatment and prevention of influenza for the 2009–2010 influenza season.
The new recommendations include the following additions aimed at reducing the likelihood of resistance and ensuring adequate antiviral drug supplies:
  • Do not use antivirals for postexposure chemoprophylaxis in healthy children or adults to manage outbreaks in the community, school, camp, or other settings.
  • Age-based dosing recommendations are provided for children younger than 1 year.
For high-risk individuals, consider:
  • Increased use of preemptive therapy after exposure with an emphasis on prompt treatment of symptomatic people in lieu of prophylaxis. (Remember that the doses for prophylaxis and therapy are different.)
  • Establishing systems to ensure rapid access to antiviral therapy when needed (e.g., providing telephone consultation and prescriptions after office hours or giving prescriptions to patients to fill if needed only after speaking with a physician).
Comment:
Pandemic influenza poses multiple challenges related to the frequency of changes in information and recommendations. These case reports and recommendations highlight the need for judicious use of antivirals in otherwise healthy individuals and rapid access to appropriate therapy in high-risk patients. Antiviral therapy is most effective when started within 48 hours after the onset of symptoms. Vaccination (when available) remains the mainstay of prevention and is far preferable to prophylaxis.


Peggy Sue Weintrub, MD

Dr. Weintrub is on the Speakers' Bureau for MedImmune (maker of FluMist) and Sanofi-Aventis (makers of standard flu vaccine).
Published in Journal Watch Pediatrics and Adolescent Medicine September 16, 2009

Citation(s):
Centers for Disease Control and Prevention (CDC). Oseltamivir-resistant 2009 pandemic influenza A (H1N1) virus infection in two summer campers receiving prophylaxis — North Carolina, 2009. MMWR Morb Mortal Wkly Rep 2009 Sep 11; 58:969.

Centers for Disease Control and Prevention (CDC). Updated interim recommendations for the use of antiviral medications in the treatment and prevention of influenza for the 2009-2010 season. Sep 8 , 2009. (http://www.cdc.gov/h1n1flu/recommendations.htm)

Aortic dissection 要用什麼檢查?



CTA, MRA, and TEE are all highly sensitive and specific modalities for diagnosing aortic dissection. Therefore, the condition of the patient, the information needed, and the resources and expertise immediately available should drive the choice of study. MRA is considered the gold standard diagnostic study and is the preferred modality for hemodynamically stable patients with suspected aortic dissection. Because of slow data acquisition and the inaccessibility of patients in the scanner, it is generally unsuited for unstable patients, including those with ongoing pain. Bedside TEE is an excellent choice for patients who are too unstable for MRA but is less effective at visualizing distal dissections. Arch aortography is generally reserved for the confirmation of questionable diagnoses or to image specific branch arteries.

簡單說:
  • 病人穩定:MRI 是金標準。
  • 病人不穩定:CTA 是金標準。
  • 病人不穩定又不能做CTA時:TEE是金標準。
  • CTA較難看清楚的地方(尤其是分枝處):用aortogram來輔助。
很棒的全文:
http://www3.interscience.wiley.com/cgi-bin/fulltext/112585678/PDFSTART

2009年9月17日 星期四

ACGME 六大核心能力

  1. 病人照護 (Patient care)
  2. 醫學知識 (Medical knowledge)
  3. 從工作中學習及成長 (Practice-based learning and improving)
  4. 人際及溝通技能 (Interpersonal and communication skills)
  5. 制度下的臨床工作 (System-based practice)
  6. 專業素養 (Professionalism)

2009年9月8日 星期二

COPD使用吸入性類固醇不增加肺炎機率

Inhaled Steroids in COPD: Is Risk for Pneumonia Really Higher?
Risk was not elevated in patients who received budesonide.

Do inhaled corticosteroids elevate risk for pneumonia in patients with chronic obstructive pulmonary disease? Several clinical trials, observational studies, and meta-analyses suggest that they do, by as much as 70%. But, in other trials, researchers have reported lower risk, and previous meta-analyses have been criticized for methodological weaknesses, such as combining trials of inhaled budesonide with those of fluticasone.

Canadian researchers pooled patient-level data from seven large clinical trials in which more than 7000 patients with COPD were randomized to inhaled budesonide or placebo, with or without the long-acting β2-agonist formoterol, for 6 to 12 months. In both groups, 3% of patients developed pneumonia; in 1% of budesonide recipients and in 2% of placebo recipients, it was a serious adverse event (i.e., causing hospitalization or death), with no significant difference between groups, before or after adjustment for potential confounders.

Comment: Budesonide is cleared more rapidly from the airways than fluticasone, and the authors speculate that this fact could help explain why pneumonia risk is not elevated with budesonide (as it seems to be with fluticasone). Surprisingly, despite high mortality associated with community-acquired pneumonia, no study has shown that fatal pneumonia is more common among patients who receive inhaled steroids, which suggests that pneumonias induced by inhaled steroids are relatively mild. An editorialist concludes that the benefits of inhaled steroids in COPD patients continue to outweigh the risks substantially.


Bruce Soloway, MD

Published in Journal Watch General Medicine September 8, 2009
  • Sin DD et al. Budesonide and the risk of pneumonia: A meta-analysis of individual patient data. Lancet 2009 Aug 29; 374:712.
  • Welte T. Inhaled corticosteroids in COPD and the risk of pneumonia. Lancet 2009 Aug 29; 374:668.

2009年9月2日 星期三

Apical Ballooning Syndrome

Features of Apical Ballooning Syndrome
Apical ballooning syndrome (also described as tako-tsubo cardiomyopathy, stress-induced cardiomyopathy, and the broken-heart syndrome) is an increasingly recognized condition that can closely mimic acute myocardial infarction. Its incidence is estimated to be 1 to 2% among patients who present with a presumed acute myocardial infarction. It classically affects postmenopausal women in the fifth to seventh decade, and the onset of the condition is often precipitated by emotional stress. Key features of apical ballooning syndrome are the absence of obstructive coronary artery disease in the setting of characteristic “ballooning” of the left ventricle from severe anteroapical akinesis and hypercontractility of the basal segments. Heart failure is present in approximately 50% of patients with apical ballooning syndrome, and cardiogenic shock occurs in up to 15%. Approximately 20% of these patients also have a transient systolic murmur associated with subvalvular pressure gradients that can mimic hypertrophic obstructive cardiomyopathy.

Diagnosis of Apical Ballooning Syndrome
Although it is critical to differentiate apical ballooning syndrome from acute myocardial infarction quickly, it can be challenging to do so. There are no electrocardiographic findings that clearly distinguish apical ballooning syndrome from acute myocardial infarction. With apical ballooning syndrome, the elevations in troponin are typically much lower than would be expected on the basis of the wall-motion abnormalities. However, it is difficult to rely on cardiac biomarkers alone, since these are often only modestly elevated during the early stages of an acute myocardial infarction. Thus, the diagnosis frequently becomes evident only in the cardiac catheterization laboratory, when no angiographically significant coronary artery disease is found. It is generally not advisable to withhold antithrombotic treatments such as heparin and aspirin while the diagnosis remains uncertain, since acute myocardial infarction is much more common. Decisions about fibrinolytic therapy are more complicated, given its associated risk of intracerebral hemorrhage. Whenever feasible, emergency coronary angiography should be performed to assist in clinical decision making.

What is the pathophysiology of apical ballooning syndrome?
A: The pathophysiology of apical ballooning syndrome has not been clearly elucidated. Leading hypotheses include transient catecholamine toxicity, aborted ST-elevation myocardial infarction with spontaneous lysis of thrombus, coronary vasospasm, and microcirculatory dysfunction. Similar wall-motion abnormalities have been seen in other states of catecholamine excess, such as subarachnoid hemorrhage and pheochromocytoma.

What is the recommended treatment for apical ballooning syndrome?
A: In patients with acute outflow tract obstruction, treatment should focus on ensuring adequate intravascular volume. Beta-blockers may also be considered in an attempt to slow the heart rate and increase the diastolic filling time. Although data from clinical trials are scant, some experts suggest treating patients with apical ballooning syndrome with beta-blockers and angiotensin-converting–enzyme inhibitors until left ventricular systolic function normalizes; it has also been hypothesized that treatment with beta-blockers may reduce the risk of recurrence (which is reported in a case series to be approximately 10%). Inotropic agents should be avoided, since they may exacerbate the outflow tract gradient. Aspirin should be considered for patients who have coexisting coronary artery disease. Some clinicians recommend anticoagulation with warfarin for several weeks in patients with severe systolic dysfunction in order to prevent left ventricular thrombus formation. In most patients with apical ballooning syndrome, the condition improves rapidly with supportive measures. Complete recovery of systolic function is typically observed within 4 to 6 weeks, and the overall prognosis tends to be excellent.

---
NEJM - Vol. 361, No. 10, September 3, 2009

2009年8月31日 星期一

H1N1個人防疫自我測試題庫-醫事人員版


----------------

資料來源:H1N1新型流感中央流行疫情指揮中心
日期:2009-08-31

檔案下載【密碼:2833....】:

2009年8月30日 星期日

H1N1 疫苗接種優先順序

中央流行疫情指揮中心針對H1N1疫苗接種優先順序目前研擬如下:
(1)醫療及防疫相關人員
(2)孕婦
(3)1-6歲之學齡前兒童
(4)7歲以上重大傷病者
(5)7-12歲國小學童
(6)13-15歲國中生
(7)16-18歲高中生
(8)19-24歲族群
(9)25歲以上患有心肺血管疾病、肝、腎及糖尿病等疾病之高危險族群
(10)25-49歲健康成年人
(11)50-64歲健康成年人
(12)65歲以上長者

2009年8月29日 星期六

急診專科:分散式訓練

急診專科:分散式訓練
  1. 超音波
  2. 影像醫學
  3. 毒物學
  4. 緊急醫療服務系統 (EMS)
內容如下:
http://jack119.org/jackdocs/tsem_training01.pdf

2009年8月28日 星期五

2009年8月25日 星期二

Confused about delirium?

Nearly a third of elderly patients admitted to hospital in the UK have acute confusion, or delirium. A third of cases could be prevented by identifying those most at risk. Diagnosis is clinical and the best assessment tool is the confusion assessment method (CAM), according to this useful review. If a, b and either c or d are present, delirium is likely:
  • a. Acute onset and fluctuating course during the day
  • b. Inattention - easily distractible or difficulty keeping track of conversationc.
  • c. Disorganised thinking - incoherent, rambling, or irrelevant conversation and unclear or illogical flow of ideasd.
  • d. Altered consciousness - hyperalert, lethargic or drowsy, stuporous or comatose.
Source: Postgraduate Medical Journal 2009;85:405-413

2009年8月21日 星期五

AOM:給或不給抗生素?

Antibiotic Use in Children with Otitis Media Increases Risk for Recurrence
Another reason to wait and see

Clinicians often prescribe antibiotics for treatment of uncomplicated acute otitis media (AOM) in children despite lack of evidence for improved outcomes. To examine the effects of antibiotic treatment on recurrence of AOM, investigators in the Netherlands surveyed parents of 240 children (age range, 6 months to 2 years) about 3 years after the children had participated in a multicenter, randomized, double-blind trial of amoxicillin (40 mg/kg/day in 3 doses) or placebo for treatment of AOM (JW Emerg Med Apr 1 2000). Seventy percent of parents returned questionnaires.

Parents reported at least one episode of AOM since the 6-month posttreatment follow-up visit significantly more often in the amoxicillin group than in the placebo group (63% vs. 43%). Even after adjustment for confounding factors, children in the amoxicillin group had 2.5 times the risk for recurrence. In sensitivity analysis among children who were not prescribed antibiotics during the 6 months after randomized treatment, the adjusted odds ratio for recurrence was 4.4. Ear, nose, and throat surgery was less likely in the amoxicillin group (21% vs. 30%). The authors note that wide confidence intervals limit interpretation of the results and caution that the findings cannot be generalized to children with underlying disease or who live in underresourced conditions.

Comment: One more nail in the coffin for antibiotic use in simple otitis media! This practice increases risk for colonization with resistant pathogens and recurrent infections in individual children and contributes to antibiotic resistance in the general population. In uncomplicated cases, reassure parents that resolution without antibiotics is the rule, not the exception, and try a "wait-and-see prescription," rather than immediately starting unnecessary antibiotics.


Kristi L. Koenig, MD, FACEP
Published in Journal Watch Emergency Medicine August 7, 2009
Citation(s): Bezáková N et al. Recurrence up to 3.5 years after antibiotic treatment of acute otitis media in very young Dutch children: Survey of trial participants. BMJ 2009 Jun 30; 338:b2525. (http://dx.doi.org/10.1136/bmj.b2525)

-----------
反對意見:

Dangerous bias - Otitis Media

Dr. Koenig:

Your comments in the August 10 issue, concerning otitis media treatment are misleading, and possibly prejudicial. You continue to provide articles of one country (Nederlands), whose definitions and standards may differ from ours – either positively or negatively. But…these reports remain, still, the claims of one country’s research.
This article cited (BMJ) does relate more recurrences with antibiotic usage. However, neither the headline, nor your comments, notes that less surgery was needed for the otitis media treated group.

Additionally, the authors themselves acknowledge "wide confidence intervals" – which may certainly influence the validity of their observations. Nor are any details provided about their “wide confidence intervals.”

The very diagnosis of otitis media is frequently incorrectly described – both here and in the Nederlands - as a red or inflamed TM in a child, instead of a clearly bulging tympanic membrane, which is immotile with pneumatic otoscopy. This review does not refer to diagnostic criteria used.

Even if these authors employ appropriate diagnostic methods and follow-up, the issue of the avoidance of surgery is very significant. That is part of the clinical equation. Does not this significant reason for treatment retain some clinical relevance?

Lastly, your reference of yet another reason to defer antibiotics in “simple otitis media” minimizes the controversy of treatment for children less than 2, at higher risk for mastoiditis. There are "data surfing" young physicians who might apply this factum, in a one-upmanship attempt to be "current", with catastrophic results for young children. Although acknowledging bacterial resistance problems, and the option of not treating children less than 2, current AAP standards and the 18th edition of Nelson by no means foreclose the option of treating these younger children. They also define otitis media by risk factors, rather than "simple otitis media", which can be construed as any otitis media without complications. Finally, their recommended dosage is 80 mg/kg/day - which has some bearing on both treatment success and the acquisition of resistant bacteria.

Even if there is some truth, your expression of "nails in the coffin" for an illness which often IS bacterial, particularly in children less than 2, and which can result in mastoiditis or worse is - in my opinion – facile and unprofessional .
You owe your readers a more nuanced evaluation of data, and I believe that you would do well to review your own critical methods.

--
Ronald S. Bashian, MD, 19 Aug 2009 12:33 PM EST
Competing interests: None declared

2009年8月18日 星期二

最重要的工具是醫師的手

二次回診病人腸炎而水瀉發燒,主訴右下腹痛20年了...。
下腹有壓痛稍偏右(說不太痛但表情像很痛),
還是切CT,手術結果真的是 appendicitis!

難怪老師都說:『診斷 append. 最重要的工具是醫師的手!』

2009年8月5日 星期三

Brain death

Brain death is considered equivalent to death in most countries, and its diagnosis means that life-support measures are appropriately discontinued. Caution is needed in predicting a poor prognosis in poorly responsive patients with anoxic–ischemic encephalopathy who do not meet brain-death criteria. In the United States, the Patient Self-Determination Act of 1991 recognizes the right of the patient to leave advance directives regarding CPR or limiting levels of care.

However, in most cases, decision making is delegated to a substitute advocate or durable power of attorney. Members of the health care team should identify and meet with the person charged with decision making early in a patient's course to explain the process by which prognosis is assessed and then follow up to present results of assessments and discuss prognosis and recommendations, including withdrawal of care, when and if appropriate.

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New England Journal of Medicine - Vol. 361, No. 6, August 6, 2009

Poor neurologic outcome after cardiac arrest

Predictors of Neurologic Outcome after Cardiac Arrest
If a patient remains comatose for more than 24 hours after resuscitation from cardiac arrest or after therapeutic hypothermia, the prognostic guidelines developed by the American Academy of Neurology should be used to assess whether the patient has a good or a poor prognosis. Clinical features predicting a poor outcome include absence of pupil or corneal reflexes; absence of noxious motor response other than extensor posturing; and myoclonic status epilepticus. If somatosensory evoked potential (SSEP) responses are absent at day 1, the measurement can be repeated at day 3 or beyond; if N20 responses (N20 is the response 20 msec after electrical stimulation) are lost, the prognosis is poor. Measurement of serum NSE, if immediately available, may also be useful in the prediction of a poor outcome, although validation is needed.

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New England Journal of Medicine - Vol. 361, No. 6, August 6, 2009

Predicting outcome after cardiac arrest

What is the role of neuroimaging in predicting neurologic outcome after cardiac arrest?
A: Computed tomographic (CT) images are usually normal immediately after a cardiac arrest, but by day 3 they often show brain swelling and inversion of the gray–white densities in patients with a poor outcome. Further study is needed to assess the clinical use of these findings in establishing prognosis. Magnetic resonance imaging (MRI) has also been proposed as a means of assessing prognosis after cardiac arrest, but limited data call its use into question. The use of apparent diffusion coefficient (ADC) mapping was reported to add greater precision in predicting a poor outcome. MR spectroscopy (e.g., for pH and N-acetylaspartate, a neuronal marker) has been reported to correlate with a poor outcome in small studies, but more data are needed. Measures of cerebral metabolism with positron-emission tomography and determination of intracranial pressure, brain oxygen, or jugular venous oxygenation have not appeared sufficiently discriminatory for a poor outcome to be clinically useful, although studies are small.

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New England Journal of Medicine - Vol. 361, No. 6, August 6, 2009

N20 response from SSEPs

What is the most accurate predictor of poor outcome in patients with anoxic–ischemic encephalopathy?
A: The measurement of somatosensory evoked potentials (SSEPs), especially the N20 response from the primary somatosensory cortex (assessed 20 msec after electrical stimulation of the median nerve at the wrist), has emerged as the most accurate predictor of a poor outcome in patients with anoxic–ischemic encephalopathy. In a meta-analysis, bilateral absence of the N20 response was associated with essentially no false positives (pooled 95% CI, 0 to 2). In some patients, N20 responses are intact at 24 hours after arrest but are lost by 72 hours; once lost, they are not regained, and outcomes are poor.

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New England Journal of Medicine - Vol. 361, No. 6, August 6, 2009

2009年7月8日 星期三

Histoplasma capsulatum


This blood smear was taken from an immunodeficient man with fever, night sweats, and weight loss. What is the diagnosis?
Ans: Histoplasma capsulatum

2009年7月3日 星期五

Ketamine and Etomidate

Ketamine and Etomidate: Good Choices for RSI in Critically Ill Patients
Mortality rates were similar in patients who received single doses of etomidate or ketamine.

Despite etomidate’s hemodynamic benefits, some clinicians have challenged its use for rapid sequence intubation (RSI) in critically ill patients, citing concerns about adrenal insufficiency (JW Emerg Med Feb 1 2008). In a prospective trial, researchers compared outcomes in 469 adult patients who were randomized to receive a single intravenous bolus of etomidate (0.3 mg/kg) or ketamine (2.0 mg/kg) for induction during RSI at 65 intensive care units (ICUs) and 12 emergency departments or prehospital systems in France. All patients received IV succinylcholine (1 mg/kg) immediately after the trial medication and continuous sedation with midazolam (0.1 mg/kg/hour) combined with fentanyl or sufentanil after tube placement was confirmed.

Final diagnoses were categorized as trauma (22%), sepsis (16%), or other (including stroke, overdose, cardiogenic shock, and acute respiratory failure; 62%). Adrenal insufficiency occurred in significantly more etomidate recipients than ketamine recipients (86% vs. 48%; odds ratio, 6.7). However, no significant differences were noted between groups in maximum sequential organ failure assessment (SOFA) scores during the first 3 days in the ICU (the primary outcome), intubation conditions, various measures of catecholamine use, or 28-day mortality. No drug-related adverse outcomes were reported with either agent. The authors conclude that "ketamine is a safe and valuable alternative to etomidate for intubation in critically ill patients, particularly in septic patients." Editorialists suggest that successful intubation depends on a solid knowledge of pharmacology but do not recommend one agent over the other.

Comment: This elegant and ambitious study demonstrated measurable adrenal suppression but no evidence of adverse outcome related to a single bolus of etomidate for RSI in patients with various types of shock. Adrenal axis suppression is common in critically ill patients; in fact, about half the patients who received ketamine had adrenal insufficiency in this study. The authors note that only 16% of study patients had septic shock, and they call for a larger randomized study that includes more patients with sepsis. Clinicians should choose induction drugs based on individual patient parameters and personal familiarity and not be dissuaded from using either etomidate or ketamine based on concerns that are not supported by evidence.


Kristi L. Koenig, MD, FACEP
Published in Journal Watch Emergency Medicine July 2, 2009

Citation(s): Jabre P et al. Etomidate versus ketamine for rapid sequence intubation in acutely ill patients: A multicentre randomised controlled trial. Lancet 2009 Jul 1; [e-pub ahead of print]. (http://dx.doi.org/10.1016/S0140-6736(09)60949-1)

Wenzel V and Lindner KH. Best pharmacological practice in prehospital intubation. Lancet 2009 Jul 1; [e-pub ahead of print]. (http://dx.doi.org/10.1016/S0140-6736(09)61071-0)

2009年6月29日 星期一

如何用FAST診斷氣胸

這是急診醫師的必備技能之一!

http://www.youtube.com/watch?v=fntJ7GLjCSU



PS: 可以用 youtube downloader 下載影片喔!

2009年6月24日 星期三

Alcoholic Hepatitis - 預後

What determines the prognosis of alcoholic hepatitis?
A: Abstinence from alcohol is the cornerstone of recovery. A promising clinical course in alcoholic hepatitis is largely dictated by abstinence from alcohol, a mild clinical syndrome, and the implementation of appropriate treatment. Within several weeks after discontinuation of alcohol intake, jaundice and fever may resolve, but ascites and hepatic encephalopathy may persist for months to years. Either continued jaundice or the onset of renal failure signifies a poor prognosis. Unfortunately, even when patients adhere to all aspects of medical management, recovery from alcoholic hepatitis is not guaranteed. Up to 40% of patients with severe alcoholic hepatitis die within 6 months after the onset of the clinical syndrome.

What is the risk of liver cirrhosis in patients with chronic excessive alcohol consumption?
A: The association between alcohol intake and alcoholic liver disease has been well documented, although cirrhosis of the liver develops in only a small proportion of heavy drinkers. The risk of cirrhosis increases proportionally with daily consumption of more than 30 g of alcohol per day; the highest risk is associated with daily consumption of more than 120 g per day. The point prevalence of cirrhosis is 1% in persons drinking 30 to 60 g of alcohol a day and up to 5.7% in those consuming 120 g per day. It is presumed that other factors, such as sex, genetic characteristics, and environmental influences (including chronic viral infection such as hepatitis C), play a role in the genesis of alcoholic liver disease.

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New England Journal of Medicine - Vol. 360, No. 26, June 25, 2009

Alcoholic Hepatitis - 臨床表現

Clinical Presentation of Alcoholic Hepatitis
Alcoholic hepatitis is a clinical syndrome of jaundice and liver failure that generally occurs after decades of heavy alcohol use. The cardinal sign of alcoholic hepatitis is the rapid onset of jaundice. Other common signs and symptoms include fever, ascites, and proximal muscle loss. Patients with severe alcoholic hepatitis may have encephalopathy. Typically, the liver is enlarged and tender.

Treatment of Alcoholic Hepatitis
General approaches for patients with decompensated liver disease include treatment of ascites (salt restriction and diuretics) and of hepatic encephalopathy (lactulose and gut-cleansing antibiotics). Infections should be treated with appropriate antibiotics, chosen according to the sensitivity of the organisms isolated. Enteral feeding may be required, as patients are often anorectic. A daily protein intake of 1.5 g per kilogram of body weight is recommended, even among patients with hepatic encephalopathy. Thiamine and other vitamins should be administered.
Delirium tremens and the acute alcohol withdrawal syndrome should be treated with short-acting benzodiazepines. The use of corticosteroids to treat alcoholic hepatitis has been controversial. Pentoxifylline, a nonselective phosphodiesterase inhibitor, decreases the transcription of tumor necrosis factor. Since TNF is elevated in alcoholic hepatitis, the agent is considered for use in some patients. Selected patients with severe alcoholic hepatitis who fail to respond to medical management should be evaluated for liver transplantation.

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New England Journal of Medicine - Vol. 360, No. 26, June 25, 2009

PCI after tPA, when?

What is the optimal time window to perform early percutaneous coronary intervention after fibrinolysis for acute myocardial infarction?

A: The time to percutaneous coronary intervention (PCI) was well under 24 hours after fibrinolysis in previous studies, and there was no difference among the trials in efficacy relative to the time to PCI. The intervals ranged from 2 to 17 hours. A two-hour interval after fibrinolysis should be considered to be the lowest acceptable interval, since PCI immediately after fibrinolysis has proven to be ineffective. An interval of 17 hours seems to be as good as PCI at 2 hours. Waiting longer than 24 hours can be disadvantageous, given the increasing risk of reocclusion of the infarct-related artery. Thus, the optimal window for early PCI after fibrinolysis is somewhere between 2 and 24 hours.

打通血管,誰較強?

What are the reperfusion rates after fibrinolysis compared to primary percutaneous coronary intervention in myocardial infarction with ST-segment elevation?

A: The goal of reperfusion therapy is early and complete recanalization of the infarct-related artery to salvage myocardium and improve both early and late clinical outcomes. Complete reperfusion can be achieved with either fibrinolysis or primary percutaneous coronary intervention (PCI). The success rate of primary PCI is higher than 90%, whereas current fibrinolytic therapy leads to full reperfusion in only 50 to 55% of recipients. Primary PCI, therefore, appears to be the most appropriate reperfusion tool, but there are substantial logistic restrictions associated with its use.

2009年6月23日 星期二

Diabetes Drugs news

New NICE guidelines in the UK on newer drugs for use in diabetes are summarised in the BMJ. Some key points are:
  1. Add sitagliptin (a DPP-4 inhibitor) as second line treatment with metformin instead of a sulphonylurea when blood glucose control is inadequate if sulphonylureas are contraindicated or if the patient is at risk of hypoglycaemia
  2. Add sitagliptin or a thiazolidinedione (pioglitazone or rosiglitazone) as a third line treatment if metformin and a sulphonylurea are not adequately controlling blood glucose and insulin is unsuitable
  3. Don't use thiazolidinediones in patients with heart failure or at high risk of fracture
  4. Add pioglitazone to insulin therapy if a thiazolidinedione has lowered blood glucose in the past or if high dose insulin is not adequately controlling blood glucose.

Source: BMJ 2009;338:b1668

2009年6月18日 星期四

毛地黃花開 勿觸摸以免中毒



記者黃玿琮/中縣報導

大雪山森林遊樂區是夏日避暑的好去處,目前區內正值毛地黃花朵綻放季節,吸引民眾上山避暑與賞花。由於毛地黃全株具有毒性,東勢林管處呼籲遊客勿採摘花朵,以免發生中毒意外。

林管處育樂課指出,花姿奇特的毛地黃因它的外觀有著茸毛密佈的莖葉及酷似地黃的葉片,故而命名為毛地黃;又名洋地黃和毒藥草、指頭花等別名,花期通常在5月至7月的時刻。是多年生而耐寒性草本植物,株高1至4尺,莖葉有毛。宛如倒掛銅鈴的花穗成串,呈現婀娜多姿,把原本翠綠的山區點綴得更嬌美,也更吸引民眾上山。

毛地黃係1910年由日本藥廠引進試種於阿里山、八仙山、大雪山、太平山、清境農場等地,海拔約二千公尺的高山,由於條件適合,目前已成為野生植物。這種「毒藥草 」全株有毒,但因性喜冷涼,栽培地區僅限於高冷地,平地栽培不易成活。

毛地黃原為藥用植物,為強心利尿藥,常用於治療充血性心衰竭和心律不整(如心房纖維顫動、心房撲動、陣發性上心室搏動過速),此兩種疾病常見於老年族群中,所以毛地黃成為老年心臟病患普遍使用的藥物之一。不過,處長陳奕煌強調,毛地黃全株具毒性,雖然是全球著名的心臟強心劑,惟需經過萃取提煉及醫師處方;遊客看到毛地黃時不宜採摘,以防中毒。

此外,遊客若有需要住宿服務,請先行電洽大雪山森林遊樂區訂妥房間,除可電話預訂外,尚有網路訂房服務,訂房網址:http://tsfs.forest.gov.tw/,大雪山國家森林遊樂區服務中心 04-25877901或04-25877902,相關旅遊資訊可上東勢林區管理處網站查詢:http://dongshih.forest.gov.tw/

2009年6月13日 星期六

正常ECG無法排除ACS

Normal ECG During Chest Pain Does Not Rule Out ACS
Among chest pain patients with normal initial ECGs, a similar percentage had acute coronary syndrome whether the ECG was performed when chest pain was present or absent.

A normal electrocardiogram does not exclude acute coronary syndrome (ACS) in patients who present with chest pain, but many clinicians believe that ACS is unlikely to be the cause of the chest pain if the normal ECG was obtained during a pain episode. To clarify this issue, these authors conducted a prospective, observational study of 387 patients who presented to an emergency department with chest pain, had normal initial ECGs, and were admitted for evaluation for ACS.

Patients were divided into two groups, based on whether they had active chest pain during acquisition of the normal initial ECG: 126 had chest pain and 261 did not. ACS was defined as non–ST-segment-elevation myocardial infarction, >70% stenosis on coronary angiography, or positive noninvasive cardiac stress test. The prevalence of ACS did not differ significantly between the groups that did and did not have chest pain when the normal initial ECG was obtained (16% and 20%).

Comment:
Lack of changes on an ECG performed during chest pain often is thought to reduce the likelihood of ACS. Findings from this and a previous study (JW Emerg Med Dec 22 2006) show that this assumption is erroneous and that, in fact, the likelihood of serious cardiac disease in patients who present with chest pain and an initial normal ECG is the same whether or not chest pain was present when the ECG was obtained.

— Diane M. Birnbaumer, MD, FACEP
Published in Journal Watch Emergency Medicine June 12, 2009

Citation(s): Turnipseed SD et al. Frequency of acute coronary syndrome in patients with normal electrocardiogram performed during presence or absence of chest pain. Acad Emerg Med 2009 Jun; 16:495.

2009年6月10日 星期三

懷孕前期使用primperan安全嗎?

The Safety of Metoclopramide Use in the First Trimester of Pregnancy

Background
In various countries, metoclopramide is the antiemetic drug of choice in pregnant women, but insufficient information exists regarding its safety in pregnancy.

Methods
We investigated the safety of metoclopramide use during the first trimester of pregnancy by linking a computerized database of medications dispensed between January 1, 1998, and March 31, 2007, to all women registered in the Clalit Health Services, southern district of Israel, with computerized databases containing maternal and infant hospital records from the district hospital during the same period. We assessed associations between the use of metoclopramide in pregnancy and adverse outcomes for the fetus, adjusting for parity, maternal age, ethnic group, presence or absence of maternal diabetes, smoking status, and presence or absence of peripartum fever.

Results
There were 113,612 singleton births during the study period. A total of 81,703 of the infants (71.9%) were born to women registered in Clalit Health Services; 3458 of them (4.2%) were exposed to metoclopramide during the first trimester of pregnancy. Exposure to metoclopramide, as compared with no exposure to the drug, was not associated with significantly increased risks of major congenital malformations (5.3% and 4.9%, respectively; odds ratio, 1.04; 95% confidence interval [CI], 0.89 to 1.21), low birth weight (8.5% and 8.3%; odds ratio, 1.01; 95% CI, 0.89 to 1.14), preterm delivery (6.3% and 5.9%; odds ratio, 1.15; 95% CI, 0.99 to 1.34), or perinatal death (1.5% and 2.2%; odds ratio, 0.87; 95% CI, 0.55 to 1.38). The results were materially unchanged when therapeutic abortions of exposed and unexposed fetuses were included in the analysis.

Conclusions
In this large cohort of infants, exposure to metoclopramide in the first trimester was not associated with significantly increased risks of any of several adverse outcomes. These findings provide reassurance regarding the safety of metoclopramide for the fetus when the drug is given to women to relieve nausea and vomiting during pregnancy.

From NEJM Volume 360:2528-2535 June 11, 2009 Number 24

------------------------

In the U.S., treatment of nausea and vomiting during early pregnancy usually involves pyridoxine (vitamin B6) and antihistamines, such as doxylamine succinate, promethazine, or meclizine. If these agents are not effective, clinicians might turn to more-potent antiemetics, such as the dopamine antagonist metoclopramide. To assess the association between metoclopramide use during early pregnancy and risk for congenital malformations, investigators linked administrative records from an Israeli HMO with medical records from the hospital at which the insured women delivered. From 1998 to 2007, 81,703 singleton live births and 998 induced abortions occurred among participants (mean age, 28; two thirds Bedouin Muslim, one third Jewish).

Among women who had singleton births and induced abortions, 4.2% and 3.8%, respectively, received first-trimester metoclopramide. Among women who had singleton births and who were exposed to metoclopramide, the rate of major congenital malformations was 5.3%; among those who were not exposed, the rate was 4.9% (adjusted odds ratio, 1.04; 95% confidence interval, 0.89–1.21). Analyses that included pregnancy terminations yielded similar findings. Early exposure to metoclopramide also was not associated with significantly altered risk for minor or multiple congenital malformations; moreover, metoclopramide showed no dose-response effect.

Comment:
Although metoclopramide is used more widely for treating women with nausea and vomiting during early pregnancy in Israel and some European countries than in the U.S., its use for this indication in the U.S. is not uncommon. Results of previous small studies have suggested that use during pregnancy is not linked to incidence of congenital anomalies. This large, retrospective cohort study provides substantial reassurance that metoclopramide does not cause congenital malformations. However, clinicians should be aware that use of this dopamine antagonist can cause maternal extrapyramidal symptoms (i.e., acute dystonic reactions and tardive dyskinesia).


Andrew M. Kaunitz, MD
Published in Journal Watch Women's Health June 10, 2009

2009年6月5日 星期五

快快壓繼續壓....很重要!

A Resuscitation Protocol That Minimizes Hands-Off Time Improves Survival
A prehospital protocol emphasizing minimal interruption of chest compressions was associated with improved survival to hospital discharge.

Recent research suggests that minimizing interruptions during cardiopulmonary resuscitation improves coronary perfusion pressure and increases the likelihood of return of spontaneous circulation (ROSC). The Kansas City, Missouri, emergency medical services system changed its cardiac arrest protocol to emphasize early chest compressions and de-emphasize airway management for resuscitation of adult patients with primary cardiac arrest (ventricular fibrillation [VF] or pulseless ventricular tachycardia). Changes included increasing the compression-to-ventilation ratio from 5:1 to 50:2 (with 200 mandatory compressions without interruption), managing the airway initially with only a nonrebreather mask followed by bag-mask ventilation, and not attempting intubation until after the third round of chest compressions or ROSC; a maximum of 10 seconds was allowed for intubation attempts.

In a retrospective study, researchers compared ROSC, survival to discharge, and cognitive function in 1097 patients with primary cardiac arrest during the 36 months before the change and 339 patients during the 12 months after. Overall, survival to discharge increased significantly from 7% before the change to 14% after (odds ratio, 1.8). In the subset of adult patients with witnessed arrest and an initial rhythm of VF (143 before the change and 57 after), survival to discharge increased significantly from 22% to 44% (OR, 2.7), and rates of ROSC increased significantly from 38% to 60% (OR, 2.4). In this subset, cerebral performance category scores at discharge (assessed only in the after group) were favorable (scores of 1 or 2) in 88% of 25 survivors.

Comment: The concept of minimally interrupted cardiac resuscitation is important for revising how we think about CPR. Our focus should be to provide sufficient and sustained perfusion to the ailing myocardium. Prolonged or repeated interruptions (e.g., frequent pulse checks or attempts to intubate) significantly undermine the process. The American Heart Association guidelines likely will be revised to incorporate this concept. In the meantime, push hard, push fast, and minimize "hands-off" time.


Aaron E. Bair, MD, MSc, FAAEM, FACEPPublished in Journal Watch Emergency Medicine June 5, 2009

Citation(s):
Garza AG et al. Improved patient survival using a modified resuscitation protocol for out-of-hospital cardiac arrest. Circulation 2009 May 19; 119:2597.

2009年6月3日 星期三

TPA After Stroke

AHA/ASA Science Advisory Recommends Use of tPA Between 3 and 4.5 Hours After Stroke

May 28, 2009 — A new science advisory from the American Heart Association (AHA)/American Stroke Association (ASA) has given the green light to the use of tissue plasminogen activator (tPA) to treat acute ischemic stroke between 3 and 4.5 hours after symptom onset.
However, the advisory, published online May 28 in Stroke, still emphasizes that time is of the essence when it comes to treatment of stroke.

"Although a longer time window for treatment has been tested formally, delays in evaluation and initiation of therapy should be avoided," the authors stress. The writing group is chaired by Gregory J. del Zoppo, MD, from the University of Washington, in Seattle.

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Susan Jeffrey
http://www.medscape.com/viewarticle/703524_print
http://stroke.ahajournals.org/cgi/reprint/40/7/2433
http://stroke.ahajournals.org/cgi/reprint/40/7/2295
http://stroke.ahajournals.org/cgi/reprint/STROKEAHA.107.181486
http://stroke.ahajournals.org/cgi/reprint/STROKEAHA.109.192535v1.pdf

2009年5月29日 星期五

Anticholinergic toxidrome

The symptoms of an anticholinergic toxidrome include blurred vision, choreoathetosis, coma, decreased bowel sounds, delirium, dry skin, fever, flushing, hallucinations, ileus, memory loss, mydriasis (dilated pupils), myoclonus, psychosis, seizures, and urinary retention. Complications include hypertension, hyperthermia, and tachycardia. Substances that may cause this toxidrome include antihistamines, atropine, benztropine, datura, tricyclic antidepressants, and scopolamine.

Due to the characteristic appearance and behavior of patients with this toxidrome, they are colloquially described as "Hot as a Hare, Dry as a Bone, Red as a Beet, Mad as a Hatter, Blind as a Bat".

Cholinergic toxidrome

The symptoms of a cholinergic toxidrome include bronchorrhea, confusion, defecation, diaphoresis, diarrhea, emesis, lacrimation, miosis, muscle fasciculations, salivation, seizures, urination, and weakness. Complications include bradycardia, hypothermia, and tachypnea. Substances that may cause this toxidrome include carbamates, mushrooms, and organophosphates.

Common mnemonics for organophosphate poisoning include the "killer B's" of bronchorrhea and bronchospasm because they are the leading cause of death, and "SLUDGE" - Salivation, Lacrimation, Urination, Diaphoresis or diarrhea, Gastrointestinal distress, and Emesis.

2009年5月27日 星期三

Hydrocortisone during Sepsis

On the basis of available evidence, current recommendations, and good clinical practice (and irrespective of the results of adrenal testing), the author, S.R. Bornstein, recommends that moderate doses of hydrocortisone (200 to 300 mg per day) should be given soon after the onset of septic shock in patients who remain hypotensive after adequate administration of fluids and vasopressor agents. Current evidence is insufficient to recommend the replacement of other steroids such as mineralocorticoids and adrenal androgens, which are also suppressed in patients with sepsis.

2009年5月26日 星期二

Kawasaki disease

Kawasaki disease-commonest cause of acquired heart disease in young children

Kawasaki disease may be rare, but it's now the commonest cause of acquired heart disease in children under 5. It's an acute, self limiting, multiorgan vasculitis of unknown cause. The problem is the vasculitis tends to affect coronary arteries and can cause sudden death if untreated. Immunoglobulins and aspirin reduce cardiac complications significantly.Diagnosis is essentially clinical-fever for five days and at least 4 of the following:Red eyes (bilateral conjunctivitis, no pus) Sore red mouth, red cracked lips, and classically a "strawberry" tongue with protuberant papillaePolymorphous maculopapular skin rashCervical lymphadenopathy, usually unilateral and >1.5 cm in diameterErythema and oedema of the hands and feet (with desquamation of the skin in the later stage of the illness).

Source: Heart 2009;95:787-792

2009年5月22日 星期五

Urine calcium oxalate crystals

What type of ingestion is accompanied by calcium oxalate crystals in the urine?
Ethylene glycol is metabolized to oxalic acid, which may combine with ionized calcium in plasma to form calcium oxalate crystals, which can be evident in the urine. Calcium oxalate can precipitate in the renal tubules and is considered to be involved in ethylene glycol-induced renal injury.

How do you calculate the osmolal gap?
A: Osmolal gap = measured serum osmolality – calculated serum osmolarity. To calculate serum osmolarity use the following formula: Serum osmolarity = ([2 × sodium] + [BUN ÷ 2.8] + [glucose ÷ 18.1]).


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New England Journal of Medicine - Vol. 360, No. 21, May 21, 2009

Ethylene Glycol Poisoning

Signs and Symptoms:
The principal clinical features of ethylene glycol poisoning are some degree of inebriation or alternation of consciousness, a profound metabolic acidosis, and acute renal failure. In severe cases, clinical hypocalcemia, multiorgan-system failure, and death occur. Methanol poisoning can cause metabolic acidosis, visual changes that may progress to blindness, and multiorgan-system failure and death. Untreated methanol poisoning is associated with a rate of death of 28% and a rate of visual deficits or blindness of 30% in survivors.


Antidotes for Methanol or Ethylene Glycol Ingestions:
Both ethylene glycol and methanol are primarily metabolized through the hepatic enzyme alcohol dehydrogenase. Either ethanol or fomepizole (4-methylpyrazole) can be used to inhibit alcohol dehydrogenase. Fomepizole was approved in the United States for the treatment of ethylene glycol poisoning in 1997; in 2000, an indication for methanol toxicity was added. Hemodialysis is an important adjunctive therapy for any ethanol-treated patient with a serum concentration of ethylene glycol or methanol of at least 50 mg per deciliter, significant academia, renal failure, or visuals signs or symptoms. Fomepizole has obviated the need for hemodialysis in many patients.

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New England Journal of Medicine - Vol. 360, No. 21, May 21, 2009

Elevated Troponin

What else can cause myocardial necrosis (and elevated serum markers) besides coronary artery disease?

Although elevated serum markers indicate myocardial necrosis, they provide no insight into its cause. In some patients, myocardial necrosis is caused by disorders other than coronary artery disease (e.g., pulmonary embolism, decompensated heart failure, severe hypertension or tachycardia, anemia, and sepsis). During evaluation of a patient with a possible acute coronary syndrome, the presence of elevated serum markers should be assessed in conjunction with other variables to provide insight into its most likely cause.

GRACE risk model

What is the GRACE risk model for patients with acute coronary syndrome?

The Global Registry of Acute Coronary Events (GRACE) risk model uses eight variables to predict whether a patient hospitalized with acute coronary syndrome will die or have a myocardial infarction in the hospital or in the next 6 months. These variables are age, Killip class (a classification of the severity of heart failure with myocardial infarction), systolic arterial pressure, ST-segment deviation, cardiac arrest during presentation, serum creatinine concentration, elevated serum markers for myocardial necrosis, and heart rate.

The application tool is available at www.outcomes-umassmed.org/grace

TIMI Risk Score

The Thrombolysis in Myocardial Infarction (TIMI) risk score uses seven variables to identify patients with acute coronary syndromes who are at risk for death, myocardial infarction, or recurrent ischemia within 14 days after hospitalization.

These include age greater than 65 years, three or more risk factors for atherosclerosis, known coronary artery disease, two or more episodes of anginal chest pain in the 24 hours before hospitalization, the use of aspirin in the 7 days before hospitalization, ST-segment deviation of 0.05 mV or more, and elevated serum markers for myocardial necrosis (troponin or creatine kinase MB).

Patients with three or more of the seven variables are considered to be at high risk, whereas those with no more than two of the variables are considered to be at low risk.

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New England Journal of Medicine - Vol. 360, No. 21, May 21, 2009

STEMI versus NSTEMI

In patients with myocardial infarction with ST-segment elevation (STEMI), in which the infarcted artery is usually occluded and there is ongoing transmural ischemia, it is well established that the earlier primary percutaneous coronary intervention (PCI) can be performed, the lower the mortality. By contrast, in patients with acute coronary syndromes without ST-segment elevation (NSTEMI) including unstable angina and myocardial infarction, the culprit artery is often patent, there is usually no ongoing transmural ischemia, and the patient often has a good response to initial medical treatment. The optimal timing of such intervention has been uncertain.

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New England Journal of Medicine - Vol. 360, No. 21, May 21, 2009