Bronchiolitis... The "Atomic Cold" Disease

In the ED we see kids with coughs and colds every day. Among those, a number of children have bronchiolitis. Few diseases have a greater effect on the health of young children than viral lower respiratory tract illness. Approximately 800,000 children in the United States, or approximately 20% of the annual birth cohort, require outpatient medical attention during the first year of life because of illness caused by respiratory syncytial virus (RSV). The simplest way to think about this disease that will help identifying children with bronchiolitis is this: Imagine an infant (or toddler) with a cold, pouring boogers from his nose, who looks sicker than the usual "cold". Yes... that's it! Think about it as the "Atomic Cold"

RSV accounts for 50 to 80% of all hospitalizations for bronchiolitis during seasonal epidemics in North America. Although the clinical features of bronchiolitis due to different viruses are generally indistinguishable, some differences in the severity of disease have been reported. For example, it has been observed that rhinovirus-associated bronchiolitis may result in a shorter length of hospitalization than bronchiolitis that is attributable to RSV. Differences in the response to medical intervention have not been identified consistently among children with bronchiolitis caused by different viruses. 

 

No available treatment shortens the course of bronchiolitis or hastens the resolution of symptoms. Therapy is supportive, and the vast majority of children with bronchiolitis do well regardless of how it is managed. The intensity of therapy among hospitalized children has been shown to have little relationship to the severity of illness. In 2015 the AAP updated its guidelines for the diagnosis and treatment of bronchiolitis. The evidence-based guidelines emphasize that a diagnosis of bronchiolitis should be based on the history and physical examination and that radiographic and laboratory studies should not be obtained routinely. Short-acting β₂-agonists, epinephrine, and systemic glucocorticoids are not recommended for the treatment of children with bronchiolitis. However, and this is my opinion only, I think these guidelines fall short in helping clinicians what to do when confronted with a sicker child with an "atomic cold". During each winter this scenario plays more than once per shift. A child who looks sick with a cold, very sonorous respirations, lots of secretions, chest sounds like a washer machine, maybe some retractions, slightly tachypeneic and with SaO2 in the low 90's or upper 80's. Sounds familiar? Of curse it does. 

Typical x-ray findings of peri-bronchial thickening

The guidelines say that nothing works. What am I supposed to do?! Should I just tell the parents "Your child has bronchiolitis, there is nothing to do, but bring him back when he turns blue". Really..?! That's just non-sense. I think that for the sake of the child, tranquility of the parents and the sanity of the practitioners; doing nothing in bronchiolitis is not an option. In my opinion every kid should received "nebulized something". There is some evidence that albuterol and steroids may work in atopic kids, that racemic epinephrine may reduce admission rates and hypertonic saline decreases length of stay. If there is increase work of breathing or the child is not responding, maybe getting an x-ray to rule out pneumonia may be helpful. Regardless of your approach, aggressive suctioning and PO challenge before disposition are mandatory. Also assess the parents. How are they managing at home? If after all is set and done, the child still looks "iffy" or there is a hint that parents won't be able to cope at home, just admit the child. We have to worry about a lot of things in the ED, sending home a potentially sick kid is something we don't need to lose sleep on.

Pictured above is the most wonderful machine and the best gift for parents with young children. If you do send the child home, make sure to go over the logistics on how to do home care, suctioning and educated parents on how to monitor the respiratory rates as well as warning signs and symptoms to bring the child back to the ED. What I usually say is this: "Your baby is a booger factory and the more mucous you suction the better he will breathe and eat. Do the nasal saline drops followed by suction before each feeding and before sleep, watch for increased work of breathing (nasal flaring, grunting and retractions) and if your baby refuses to eat or drink, or you are concerned or have any questions, just bring him back. Remember to wash your hands well and often, no smoking around and keep other young children away".

Happy new year to everyone; and thank you for taking care of the little patients!

Chest Compression During CPR ... Don't Forget The Brain !

Chest compression are the core of resuscitation efforts in any patient with confirmed or suspected cardiac arrest. Good CPR should not be thought as heart-only process, but a combination of heart and brain.   Standard cardiopulmonary resuscitation consists of manual chest compressions to maintain blood flow and positive-pressure breathing to maintain oxygenation until spontaneous circulation is restored. Chest compressions are interrupted frequently by ventilations given as rescue breathing during the treatment of out-of-hospital cardiac arrest. These interruptions reduce blood flow and potentially reduce the effectiveness of CPR. Observational studies involving humans with out-of-hospital cardiac arrest of presumed cardiac cause have suggested that continuous compressions are associated with better survival than interrupted compressions. Nichol et al. conducted a randomized trial to test whether continuous chest compressions, as compared with chest compressions interrupted for ventilation, during CPR performed by emergency medical service (EMS) providers affected the rate of survival, neurologic function, or the rate of adverse events. In the large randomized trial conducted by Nichol et al. involving adults with out-of-hospital cardiac arrest, a strategy of continuous manual chest compressions with positive-pressure ventilation was not associated with a significantly higher rate of survival to discharge. During the active-enrollment phase, 1129 of 12,613 patients (9.0%) in the intervention group (which received continuous chest compression) and 1072 of 11,035 (9.7%) in the control group (which received interrupted chest compressions) survived to hospital discharge (difference with adjustment for cluster and sequential monitoring, −0.7 percentage points; 95% confidence interval [CI], −1.5 to 0.1; P=0.07). In the study by Nichol et al., secondary outcomes included neurologic function at discharge, which was measured with the use of the modified Rankin scale (scores range from 0, indicating no symptoms, to 6, indicating death, with a score of ≤3 indicating favorable neurologic function) on the basis of review of the clinical record, and adverse events. Among patients with available data on neurologic status, 883 of 12,560 patients (7.0%) in the intervention group and 844 of 10,995 (7.7%) in the control group survived with a modified Rankin scale score of 3 or less (difference with adjustment for cluster, −0.6 percentage points; 95% CI, −1.4 to 0.1; P=0.09). Hospital-free survival in the Nichol trial was defined as the number of days alive and permanently out of the hospital during the first 30 days after the cardiac arrest. Hospital-free survival was significantly shorter in the intervention group than in the control group (mean difference, −0.2 days; 95% CI, −0.3 to −0.1; P=0.004). Previous observational studies have shown large increases in survival rates among patients with a shockable rhythm with the implementation of continuous compressions by EMS providers versus compressions interrupted for ventilations. Among patients with a noncardiac cause of cardiac arrest who were treated by laypersons or those with a nonshockable rhythm who were treated by EMS providers, continuous compressions were not associated with a significant improvement in outcome. In these previous studies, participating EMS agencies did not measure CPR process when implementing continuous compressions, and implementation occurred simultaneously with other changes, including directions to give intravenous epinephrine early, to use a nonrebreather mask with passive ventilation, to defer airway insertion, and to reduce the number of defibrillations given with each rhythm analysis. In the initial reports of implementation of continuous compressions, most patients received rescue breathing by means of positive-pressure ventilation with a bag-valve mask. Other interventions that each patient received were not reported. It seems plausible that some of the observed improvement in these previous studies was due to improved CPR process (e.g., compression rate and depth), concurrent improvements in the system of care, or Hawthorne effects (changes in behavior resulting from awareness of being observed) rather than to the implementation of continuous compressions alone. In Summary... - Rapid initiation of chest compression increases survival with better neurological outcome. - Avoiding interruptions during chest compression is key for brain perfusion. - Defibrillate for shockable rhythms.  - Teaching the general public on how to do high quality chest compressions can make a real difference.

DVT and Pregnancy

Although the absolute incidence of venous thromboembolism in pregnancy is low (1 or 2 cases per 1000 pregnancies), this risk is approximately five times as high as the risk among women who are not pregnant. These risks reflect the venous stasis and procoagulant changes in coagulation and fibrinolysis, which are considered to be part of physiologic preparation for the hemostatic challenge of delivery.

The clinical diagnosis of venous thrombosis is unreliable in pregnancy. Suggestive symptoms and signs, such as leg swelling and dyspnea, may be difficult to differentiate from the physiologic changes of pregnancy. As compared with deep-vein thrombosis in nonpregnant persons, deep-vein thrombosis in pregnant women occurs more frequently in the left leg (85%, vs. 55% in the left leg among nonpregnant persons) and is more often proximal (72% in the iliofemoral veins, vs. 9% in the iliofemoral veins among nonpregnant persons), with a greater risk of embolic complications and the post-thrombotic syndrome. Thrombotic events occur throughout pregnancy, with more than half occurring before 20 weeks of gestation. The risk increases further in the puerperium (the 6-week period after delivery), probably owing to endothelial damage to the pelvic vessels that occurs during delivery. Recent data indicate that an increased relative risk (but low absolute risk) persists until 12 weeks after delivery. However, approximately 80% of postpartum thromboembolic events occur in the first 3 weeks after delivery.

Suspected deep-vein thrombosis is best assessed by means of compression duplex ultrasonographic examination, including examination of the iliofemoral region. In women with a negative result on ultrasonography in whom clinical suspicion of deep-vein thrombosis is high, it may be prudent to repeat the test after 3 to 7 days. In cases in which iliocaval venous thrombosis is suspected but ultrasonography cannot detect a thrombus, magnetic resonance or conventional x-ray venography may be considered. Chest radiographic findings are normal in the majority of cases of pulmonary embolism, but they can show pulmonary features that point to an alternative diagnosis or nonspecific features of pulmonary embolism such as atelectasis or regional oligemia. Since deep-vein thrombosis is often present in patients with pulmonary embolism, ultrasonographic venography is useful in patients who have possible symptoms or signs of deep-vein thrombosis. If deep-vein thrombosis is detected, further radiologic studies do not have to be performed to confirm a pulmonary embolism. In women with normal findings on chest radiography, ventilation–perfusion lung scanning is often recommended, since it has a high negative predictive value, owing to the low prevalence of coexisting pulmonary problems that can result in indeterminate or false positive results. Moreover, the ventilation component can often be omitted, thereby minimizing the dose of radiation to the fetus. Whereas computed tomographic (CT) pulmonary angiography (CTPA), with its high sensitivity and specificity, is usually the first-line test to detect pulmonary embolism in nonpregnant patients, it is used less often in pregnant women.

One diagnostic study frequently used is the D-dimer. Pregnancy is a hyper coagulable state and therefore, D-dimer need to be adjusted. There is growing evidence that trimester adjusted D-dimer is safe, reduces testing without missing more clots. 1st trimester cut off can be 50% more than the normal laboratory value, during the 2nd trimester 100% and 3rd trimester 150% the normal value. Of note, D-dimers normalize to the pre-pregnancy value after 4-6 weeks.

Anticoagulation in pregnancy typically involves unfractionated heparin or low-molecular-weight heparin, which do not cross the placenta or enter breast milk. In contrast, vitamin K antagonists such as warfarin are contraindicated in pregnancy, since they cross the placenta and their use is associated with embryopathy, central nervous system abnormalities, pregnancy loss, and fetal anticoagulation with possible bleeding. Low-molecular-weight heparins have largely replaced unfractionated heparin for the management of venous thromboembolism in pregnancy. Typical agents include dalteparin (at a dose of 200 IU per kilogram of body weight daily or 100 IU per kilogram twice daily), enoxaparin (1.5 mg per kilogram daily or 1 mg per kilogram twice daily), and tinzaparin (175 units per kilogram daily). Data are limited regarding the use of fondaparinux in pregnancy. Oral direct thrombin inhibitors such as dabigatran and anti–factor Xa inhibitors such as rivaroxaban should generally be avoided during pregnancy. These agents may cross the placenta with possible adverse fetal effects. Thrombolysis in pregnancy is reserved for massive life-threatening pulmonary embolism with hemodynamic compromise or for proximal deep-vein thrombosis that is threatening leg viability. Caval filters are sometimes used in women who have recurrent pulmonary embolisms despite adequate anticoagulation or in whom anticoagulation is contraindicated, or in women in whom acute deep-vein thrombosis has developed close to the time of delivery.

Women should be advised to discontinue injections of heparin if labor starts or is suspected. Neuraxial anesthesia is usually deferred until at least 24 hours after the last dose, given a small risk of epidural hematoma associated with administration of neuraxial anesthesia before that time. After delivery, low-molecular-weight heparin should not be administered for at least 4 hours after spinal anesthesia or removal of an epidural catheter. After delivery, anticoagulant treatment is continued for at least 6 weeks, with a minimum total duration of 3 months.

Heparin Induced Thrombocytopenia

Although the use of heparin is relatively common in the ED, rarely we encounter this complication. In contrast to other conditions caused by enhanced consumption, impaired production, or destruction of platelets, which lead to bleeding complications, immune-mediated heparin-induced thrombocytopenia (HIT) does not induce bleeding but rather results in a paradoxical prothrombotic state. Thromboembolic complications develop in approximately 50% of patients with confirmed HIT. Venous thrombosis of the large vessels of the lower limbs and pulmonary embolism are the most frequent complications, followed by peripheral arterial thrombosis and then stroke; myocardial infarction is uncommon.

HIT occurs in approximately 1 in 5000 hospitalized patients. The risk of HIT depends on the type of heparin and the patient population. The incidence is up to 10 times as high among patients receiving unfractionated heparin as it is among those receiving low-molecular-weight heparin, and HIT occurs more frequently among patients who have had major surgery than among those who have had minor surgery or are receiving medical therapy. HIT is rare in obstetrical patients, although in contexts other than pregnancy, women are at slightly higher risk than men.

The onset of HIT characteristically occurs between 5 and 10 days after heparin is started, both in patients who receive heparin for the first time and in patients with reexposure. However, there are exceptions. In persons who have received heparin within the previous 90 days (especially, ≤30 days), there may be persistent circulating anti–platelet factor 4 (PF4)–heparin antibodies, and HIT can start abruptly on reexposure to heparin (rapid-onset HIT); in this case, HIT is sometimes complicated by an anaphylactoid reaction within 30 minutes after a heparin bolus. The fall in platelet count in HIT occurs rapidly (over a period of 1 to 3 days) and is assessed relative to the highest platelet count after the start of heparin. The typical nadir is 40,000 to 80,000 platelets per cubic millimeter, but the count may remain in the normal range (e.g., a decline from 500,000 to 200,000 per cubic millimeter). In less than 10% of patients, the decrease in platelet count is less pronounced (30 to 50% of the highest preceding value). Rarely, the platelet count may fall below 20,000 per cubic millimeter, especially when HIT is associated with other causes of thrombocytopenia, such as consumptive coagulopathy.

Although monitoring of platelet counts facilitates the recognition of HIT, it is difficult to justify in many patients, especially outpatients. Monitoring should be considered when the risk of HIT is relatively high (>1%), such as among patients who have undergone cardiac surgery and those receiving unfractionated heparin after major surgery (other than heparin received for intraoperative flushes or catheter-related flushes). Scoring systems can be helpful in estimating the probability of HIT. A widely used scoring system is the 4T score, which evaluates four indicators: the relative platelet-count fall, the timing of the onset of the platelet-count fall, the presence or absence of thrombosis, and the likelihood of another cause, with scores on the individual components ranging from 0 to 2 and higher scores indicating a higher likelihood of HIT. For those whose score is intermediate or high, laboratory tests are needed to rule out HIT. Anti–PF4–heparin enzyme immunoassays have an excellent negative predictive value (98 to 99%) but a low positive predictive value, owing to the detection of clinically insignificant anti–PF4–heparin antibodies. Diagnostic accuracy for HIT is improved with the use of both an anti–PF4–heparin enzyme immunoassay and a functional test (e.g., a platelet-activation assay).

Key interventions in patients with highly suspected or confirmed acute HIT are the prompt cessation of heparin (if still being administered) and the initiation of an alternative anticoagulant at a therapeutic dose. Prophylactic-dose anticoagulation is insufficient to compensate for massive thrombin generation, even if the patient has no apparent thrombosis. Vitamin K antagonists (e.g., warfarin and phenprocoumon) must not be given until HIT has abated (e.g., the platelet count has increased to >150,000 per cubic millimeter at a stable plateau for 2 consecutive days), because they increase the risk of venous limb gangrene and limb loss by decreasing the level of protein C. Two drugs are approved for the treatment of HIT — the direct thrombin inhibitor argatroban (in the United States, Canada, the European Union, and Australia) and the antithrombin-dependent factor Xa inhibitor danaparoid (in Canada, the European Union, and Australia). Argatroban is frequently used in critically ill patients. It has a relatively short half-life, which is independent of renal function, but it requires intravenous administration. Fondaparinux and bivalirudin are also used in this context, although they have not been approved by the Food and Drug Administration for this indication. Prophylactic platelet transfusions should be avoided in patients with HIT. The risk of bleeding is very low, and such transfusions can increase the risk of thrombosis.

Potassium metabolism... enough to make you go Bananas!

Potassium metabolism is one of those things we just have to know. We can really hurt people if get this one wrong. Here is a review on the topic. Now, go a eat some bananas ! The plasma potassium level is normally maintained within narrow limits (typically, 3.5 to 5.0 mmol per liter) by multiple mechanisms that collectively make up potassium homeostasis. Such strict regulation is essential for a broad array of vital physiologic processes. The importance of potassium homeostasis is underscored by the well-recognized finding that patients with hypokalemia or hyperkalemia have an increased rate of death from any cause. In addition, derangements of potassium homeostasis have been associated with pathophysiologic processes, such as progression of cardiac and kidney disease and interstitial fibrosis. External potassium homeostasis regulates renal potassium excretion to balance potassium intake, minus extrarenal potassium loss and correction for any potassium deficits. External potassium balance involves three control systems. Two systems can be categorized as “reactive,” whereas a third system is considered to be “predictive.” A negative-feedback system reacts to changes in the plasma potassium level and regulates the potassium balance. Potassium excretion increases in response to increases in the plasma potassium level, leading to a decrease in the plasma level. A reactive feed-forward system that responds to potassium intake in a manner that is independent of changes in the systemic plasma potassium level has also been recognized. A predictive system appears to modulate the effect of reactive systems, enhancing physiologic mechanisms at the time of day when food intake characteristically occurs — typically, during the day in humans and at night in nocturnal rodents. This predictive system is driven by a circadian oscillator in the suprachiasmatic nucleus of the brain and is entrained to the ambient light–dark cycle. The central oscillator (clock) entrains intracellular clocks in the kidney that generate the cyclic changes in excretion. When food intake is evenly distributed over 24 hours, and physical activity and ambient light are held constant, this system produces a cyclic variation in potassium excretion. Internal potassium homeostasis is the maintenance of an asymmetric distribution of total body potassium between the intracellular and extracellular fluid (approximately 98% intracellular and only a small fraction, approximately 2%, extracellular), which occurs by the balance of active cellular uptake by sodium–potassium adenosine triphosphatase, an enzyme that pumps sodium out of cells while pumping potassium into cells (called the sodium–potassium pump rate), and passive potassium efflux (called the leak rate). Little increase in the plasma potassium level occurs during potassium absorption from the gut in normal persons owing to potassium excretion by the kidney and potassium sequestration by the liver and muscle. Insulin, catecholamines, and mineralocorticoids stimulate potassium uptake into muscle and other tissues. Between meals, the plasma potassium level is nearly constant, as potassium excretion is balanced by the release of sequestered intracellular potassium. The healthy kidney has a robust capacity to excrete potassium, and under normal conditions, most persons can ingest very large quantities of potassium (400 mmol per day or more) without clinically significant hyperkalemia. Potassium that is filtered at the glomerulus is largely reabsorbed in the proximal tubule and the loop of Henle. Consequently, the rate of renal potassium excretion is determined mainly by the difference between potassium secretion and potassium reabsorption in the cortical distal nephron and collecting duct. Both of these processes are regulated — potassium ingestion stimulates potassium secretion and inhibits potassium reabsorption. Factors that regulate potassium secretion and reabsorption can be divided into those that serve to preserve potassium balance (homeostatic) and those that affect potassium excretion without intrinsically acting to preserve potassium balance (contra-homeostatic). Examples of the latter include flow rate in the renal tubular lumen and the luminal sodium level. The acid–base balance also affects potassium excretion. The predominant effect of acidosis is to inhibit potassium clearance, whereas the predominant effect of alkalosis is to stimulate potassium clearance. In vertebrates, a central clock in the suprachiasmatic nucleus of the brain and peripheral clocks that are present in virtually all cells regulate circadian rhythms. Among the many physiologic functions in humans that show circadian rhythms, few are more consistent and stable than the circadian rhythm of urinary potassium excretion. The timing signals from the central clock to the peripheral clocks remain uncertain, but adrenal corticosteroids and agents from other loci have been proposed or identified. Although the action of cortisol in promoting potassium excretion would suggest a direct (nonclock) hormonal effect, studies by Moore-Ede and colleagues indicate that cortisol serves as a clock synchronizer. Aldosterone also affects certain circadian clocks and, in particular, acutely induces the expression of period circadian clock 1 (PER1) in the kidney. Having a basic understanding of the metabolism of this mineral is important when deciding therapies to treat or prevent potassium plasma level variations. Now you know... be careful when writing for potassium or telling patients to take supplements.

PID is not just an STD, get help from your GYN.

Yes, we do see pelvic pain in the ED (a lot of them), and pelvic inflammatory disease is not an uncommon cause of many of those cases. PID is an infection-induced inflammation of the female upper reproductive tract (the endometrium, fallopian tubes, ovaries, or pelvic peritoneum). Many women have clinically silent spread of infection to the upper genital tract, which results in subclinical pelvic inflammatory disease. Pelvic inflammatory disease is a major concern because it can result in long-term reproductive disability, including infertility, ectopic pregnancy, and chronic pelvic pain.

More than 85% of infections are due to sexually transmitted cervical pathogens or bacterial vaginosis–associated microbes, and approximately 15% are due to respiratory or enteric organisms that have colonized the lower genital tract. Ascending infection from the cervix is often due to sexually acquired infections with Neisseria gonorrhoeae or Chlamydia trachomatis. Acute pelvic inflammatory disease has classically been defined by the abrupt onset of severe lower abdominal pain during or shortly after menses, although it is now well recognized that both the onset and severity of symptoms can be more ill-defined and subtle. Atypical, milder clinical manifestations have become more common as rates of N. gonorrhoeae infection have fallen. The symptoms associated with acute pelvic inflammatory disease include pelvic or lower abdominal pain of varying severity, abnormal vaginal discharge, intermenstrual or postcoital bleeding, dyspareunia, and dysuria. Fever can occur, but systemic manifestations are not a prominent feature of pelvic inflammatory disease.

The clinical diagnosis of pelvic inflammatory disease is based on the finding of pelvic organ tenderness, as indicated by cervical motion tenderness, adnexal tenderness, or uterine compression tenderness on bimanual examination, in conjunction with signs of lower genital tract inflammation. Signs of lower genital tract inflammation include cervical mucopus, which is visible as an exudate from the endocervix or as yellow or green mucous on a cotton-tipped swab placed gently into the cervical os (positive “swab test”); cervical friability (easily induced columnar epithelial bleeding); or increased numbers of white cells observed on saline microscopic examination of vaginal secretions (wet mount). All patients with suspected pelvic inflammatory disease should undergo cervical or vaginal nucleic acid amplification tests for N. gonorrhoeae and C. trachomatis infection; if the results are positive, the probability that pelvic inflammatory disease is present increases substantially. Transvaginal ultrasonography and magnetic resonance imaging (MRI) revealing thickened, fluid-filled tubes are timely and highly specific for salpingitis. However, the sensitivity of ultrasonography is only fair, and although MRI has high sensitivity, it is expensive and not typically available in resource-poor settings. Power Doppler studies showing increased fallopian-tube blood flow are highly suggestive of infection.

Most patients are successfully treated as outpatients with single-dose intramuscular ceftriaxone, cefoxitin plus probenicid, or another third-generation cephalosporin (cefotaxime or ceftizoxime), followed by oral doxycycline with or without metronidazole for 2 weeks. For hospitalized patients, therapy with cefotetan or cefoxitin (administered parenterally until 24 to 48 hours after clinical improvement) together with doxycycline and followed by doxycycline with or without metronidazole to complete 2 weeks of treatment is recommended. An alternative regimen of clindamycin and an aminoglycoside may be particularly appropriate for patients with a tubo-ovarian abscess. Adjunctive nonsteroidal anti-inflammatory drugs do not improve the clinical outcome. Removal of an intrauterine device (IUD) does not hasten clinical resolution (and may delay it), and in most cases the IUD is left in place.

Although more than 90% of patients with pelvic inflammatory disease will have a clinical response to CDC-recommended treatment, the long-term outcome of treatment is still suboptimal. It remains unclear why the long-term outcome of treated pelvic inflammatory disease remains so dismal, given the high rates of clinical response. Perhaps infection-induced damage to the fallopian tubes has occurred by the time treatment is first given. This observation, together with the frequent occurrence of subclinical pelvic inflammatory disease, have highlighted the importance of recognizing prevention of pelvic inflammatory disease as a major public heath priority. The U.S. Preventive Services Task Force, CDC, and other professional organizations recommend annual C. trachomatis screening for all sexually active women younger than 25 years of age and older women at increased risk for infection (e.g., women with multiple or new sex partners). These groups also recommend testing for N. gonorrhoeae among women at increased risk for infection (e.g., women with multiple sex partners or previous gonorrhea infection and women living in communities with a high prevalence of disease).

Oxygen IS a drug, use it with caution, only when is needed.

This is a quick review on the potentially harmful effects of too much oxygen, published in this month's EPM magazine. 

THE POTENTIAL HARM OF OXYGEN THERAPY IN MEDICAL EMERGENCIES
Cornet, A.D., et al, Crit Care 17(2):313, April 18, 2013
These Dutch authors comment on possible harm from routine use of supplemental oxygen in patients with a medical emergency. Several early studies reported high-flow oxygen in myocardial infarction patients was associated with reduced cardiac output and stroke volume with an increase in systemic vascular resistance and arterial blood pressure, largely due to vasoconstriction, with no evidence of a benefit of hyperoxia on myocardial ischemia. Clinical trials of supplemental oxygen in patients with cardiac emergencies are limited, but a 2010 Cochrane review reported increased mortality in MI patients receiving supplemental oxygen (RR 3.0). Experimental evidence also suggests an adverse hemodynamic effect of oxygen in patients with congestive heart failure. The adverse effects of supplemental oxygen are more widely appreciated in patients with chronic obstructive pulmonary disease (COPD), and a recent randomized trial noted decreased mortality in COPD patients receiving titrated rather than high-concentration oxygen. 

Hyperoxia in stroke has been noted to be associated with a decrease in cerebral blood flow and increased mortality, and use of supplemental oxygen for most ischemic stroke patients is not supported in American Stroke Association guidelines. Several large studies reported increased mortality and poor neurologic outcomes in hyperoxic patients after resuscitation from cardiac arrest. Although it is possible that vasoconstriction due to hyperoxia might be beneficial in patients with shock, no studies have demonstrated a benefit of supranormal oxygen levels in this setting. The authors advise caution with the routine use of supplemental oxygen for medical emergencies. While hypoxemia should be treated promptly, they recommend slow stepwise titration and feel that an oxygen saturation of 90-94% may be reasonable. 61 references (cornet@vumc.nl – no reprints)

Conclusions:
- Oxygen IS toxic when used in high concentrations and for prolonged periods of time.
- Hyperoxia causes cellular dysfunction 
- Use it only when patient is hypoxic and when hypoxia has been corrected, titrate down to maintain normoxia.
- Share the knowledge and stop the ritual of putting every patient on oxygen !