Monday, April 14, 2014

Hypersensitivity to Hymenoptera Sting... Not a Little Problem !

Spring is here and with that, the return of the hymenoptera stings coming to the ER. So we are going to review this week's NEJM article on the topic using the question and answer format.

What is the antigenic cross-reactivity between Hymenoptera species?
The Hymenoptera insects whose stings cause allergy are generally from three families: Apidae (honeybees and bumblebees), Vespidae (hornets, wasps, and yellow jackets), and Formicidae (fire ants). The molecular characteristics of the venoms from the three families of Hymenoptera are sufficiently different that there is very little antigenic cross-reactivity. Within families (e.g., vespids), there can be substantial cross-reactivity among the allergens present in the venoms; however, honeybee and bumblebee allergies are distinct.

What is the pathophysiology of an allergic reaction to a hymenoptera sting, and how common is an anaphylactic reaction?
In sensitized persons, a sting can cause the injected venom to bind to venom-specific IgE on mast cells, cross-linking high-affinity IgE receptors and subsequently leading to the rapid release of mast-cell mediators, including histamine, leukotrienes, prostaglandins, and platelet-activating factor. The released mast-cell mediators can cause a spectrum of allergic reactions, from local reactions (affecting small or large [≥10 cm] areas) or urticaria to anaphylaxis and even death. Patients with large local reactions usually do not have a systemic reaction to subsequent stings (with systemic reactions occurring in <10% of these patients), nor do children with isolated urticaria. However, a previous systemic reaction in a patient with venom-specific IgE is associated with a high risk of subsequent systemic reaction, which may occur in 30 to 60% of these patients. Anaphylaxis due to a hymenoptera sting causes at least 40 deaths per year in the United States, although this number is probably an underestimate. Severe systemic allergic reactions occur in approximately 0.4 to 0.8% of children and 3.0% of adults.

What are the risk factors for a severe reaction to a hymenoptera sting and how should it be treated?
Acute systemic reactions typically occur very rapidly after a hymenoptera sting but may be delayed for several hours or be biphasic. The factors associated with an increased risk of severe reaction include being stung by a honeybee (greater risk than with other hymenoptera), underlying mast-cell disorders with elevated serum-tryptase levels at baseline, a previous severe reaction, preexisting cardiovascular disease, and concomitant treatment with a beta-blocker, angiotensin-converting–enzyme inhibitor, or both. Anaphylaxis can present with a spectrum of signs and symptoms affecting multiple organ systems, including the skin, gastrointestinal tract, cardiovascular system, nervous system, and both the upper and lower respiratory tracts; hallmarks of anaphylaxis are the development of hypotension or the involvement of more than one organ system. The treatment of anaphylaxis in the emergency department should include epinephrine for any patient who has more than cutaneous symptoms; epinephrine should also be considered in adults with urticaria alone. H1-antihistamines can help relieve cutaneous signs and symptoms. For respiratory symptoms, supplemental oxygen and inhaled beta2-agonists should be used. For patients with hypotension, volume resuscitation is indicated, with 1 to 2 liters of 0.9% (isotonic) saline infused rapidly (e.g., a dose of 5 to 10 ml per kilogram in the first 5 to 10 minutes in an adult, and 10 ml per kilogram in a child).

Who should receive venom immunotherapy?
Subcutaneous immunotherapy should be considered in all patients who have had a systemic allergic reaction to an insect sting and who have a positive skin test or a positive result on an in vitro test for venom-specific IgE antibodies. Children 16 years of age or younger who have had isolated cutaneous systemic reactions to insect stings have a very low risk of subsequent reactions and do not require venom immunotherapy. Venom immunotherapy is also generally not necessary in patients who have had only a large local reaction, because their risk of subsequent systemic reactions is relatively low. However, patients with unavoidable or frequent exposures (e.g., beekeepers) may benefit, because observational data indicate that, after immunotherapy, local reactions are reduced in size and duration.

Key points to remember:
- Hymenoptera stings CAN kill, so take them seriously, specially those with prior severe reactions and honeybee stings.
- It is an IgE hypersensitivity reaction, therefore it is fast in most cases, but don't forget it can be biphasic.
- High risk are patients on beta blockers, ACEI and cardiovascular disease, the very young and old.
- Anaphylaxis is hypotension plus one other system involved: Skin, GI, respiratory or neurologic. Don't miss it !
- If it looks bad... IS bad. Get epinephrine IM mas rapido and quickly start an epinephrine drip and ensure good volume resuscitation. Antihistaminics, steroids and beta agonist are secondary agents.
- Arrange for follow up in all severe cases for possible immunotherapy, let the PCP and allergist make that call.
- Don't forget your dog... consult the vet right away! '',

Thursday, March 13, 2014

Management of Skin Abscesses. NEJM review article

From this week's NEJM... some guidelines in how to treat this common problem.

Clinical Pearls
How does ultrasound enhance the diagnostic accuracy of physical exam in detection of an abscess?
Studies in adults and children suggest that soft-tissue ultrasonography enhances the diagnostic accuracy of abscess detection and alters plans for management that are based on physical examination alone. In a prospective study involving 126 adults with clinical cellulitis in whom an emergency physician believed an abscess was not obvious on physical examination but might be present, ultrasonography resulted in a change in projected management in 56% of the patients. Ultrasonographic images showed fluid collection that was consistent with an abscess in half these patients, and approximately 80% of patients who underwent additional diagnostic testing had pus or other fluid collections. Management was also altered in three quarters of patients in whom drainage had been thought to be required on the basis of physical examination alone (e.g., it was decided that drainage was not needed, that further imaging was required, or that the incision and drainage approach should be altered).
What are the general principles of incision and drainage of an abscess in the office setting?
Many abscesses can be managed in the office setting by a general practitioner. Large, complex, or recalcitrant abscesses, especially those over sensitive areas (e.g., the hands or face), should prompt consideration of referral to a specialist or an emergency department, where additional resources can be brought to bear. The primary treatment for skin abscesses is incision and drainage. A single incision is made; the incision should be long enough to ensure complete drainage, allow lysis of loculations with a blunt instrument, and follow tension lines in order to minimize scarring. A common mistake is to make an incision that is not deep enough to reach and fully drain the abscess cavity. Particular care should be taken before incising the skin over critical structures, such as major vessels and nerves. A recent small study among adults suggested that many abscesses can be adequately drained through a short incision (median length, 1 cm).
Q. According to the authors, when should primary closure of drained abscesses be considered?
A. Primary closure of drained abscesses should be considered for large incisions (i.e., >2 cm), especially over cosmetically important areas, and may warrant referral to a specialist. Primary closure should not be performed in patients with infected sebaceous cysts or lymph nodes or similar disease processes, patients in whom the adequacy of drainage is in doubt, and patients who have systemic infection or a strong risk factor for systemic infection (e.g., diabetes).
Q. When is antibiotic treatment recommended in addition to incision and drainage of an abscess, and in such cases, what is the appropriate antibiotic regimen?
A. The Infectious Diseases Society of America (IDSA) recommends systemic antibiotic treatment, in addition to incision and drainage, for patients with severe or extensive disease (e.g., multiple sites of infection) or with rapid disease progression and associated cellulitis, signs and symptoms of systemic illness, associated coexisting conditions or immunosuppression, very young age or advanced age, an abscess in an area difficult to drain (e.g., face, hands, or genitalia), associated septic phlebitis, or an abscess that does not respond to incision and drainage alone. Empirical antibiotic therapy, if prescribed, should have in vitro activity against community-associated MRSA. Most patients who have a minor abscess can be treated as outpatients with inexpensive oral antibiotics. TMP-SMX, clindamycin, and tetracycline have been shown to have in vitro activity against 94% to nearly 100% of more than 300 MRSA isolates tested in a 2008 U.S. emergency department–based surveillance study. Other antibiotics with anti-MRSA activity that have been approved by the Food and Drug Administration for the treatment of skin and soft-tissue infection include vancomycin, linezolid, daptomycin, telavancin, tigecycline, and ceftaroline.

Worth emphasizing:
1) Incision and drainage is the primary treatment for skin and soft tissue abscess.
2) Consider referring if abscess is located in complicated or cosmetically sensitive areas.
3) Antibiotics ONLY for complicated or high risk cases.
4) Cheap antibiotics are just fine.


In another note… I want to thank my new friends at Cho Ray Hospital in Ho Chi Minh City for hosting such a great event. I look forward to next year’s conference.

Thursday, January 30, 2014

DKA and Cerebral Edema. Are Fluids to Blame or is it Shock?

It's almost the end of the month and I am again behind schedule. But today I have something controversial and very interesting... Pediatric DKA. In particular the issue about fluid administration and risk for cerebral edema.

Pedi DKA is scary, dangerous and subject of heated debate when it comes to fluid administration. Most of the treatment protocols in pediatrics are very stingy when it comes to fluid administration. In severe cases, kids arrive in shock, hypotensive, tachycardic, severely vasoconstricted, and many of them comatose; the protocol says to give them just 10 ml/kg bolus and correct remaining deficits over 48 hrs. This doesn't make  sense to me. If you are in shock, you are not perfusing! Why would I want to drag the treatment of someone in shock? I have seen my fare share of sick pedi DKA's and the ones in the severe end of the spectrum look just like that, awful. In England you cannot give a 20 ml/kg initial bolus to a DKA kid in shock without being called to the medical director office and ordered to memorize the protocol and recite it the next day in front of everyone to hear.  The notion that rapid fluid administration is the cause of cerebral edema in severe DKA is so engraved in all the treatment protocols, but there is no solid evidence to support this idea, except for observational studies and consensus recommendations. I was really bothered by this and tried to find the science behind and found that it is not the fluid rate what is associated to the risk of cerebral edema, is the level of dehydration, acidosis with hypocapnia, hyperglycemia and brain hypoperfusion what causes all the problems. The kids who are going to develop cerebral edema are in the sickest end of the spectrum, probably arrive with cerebral edema and will become clinically obvious regardless of the fluid infusion rate. 

Last year, in the journal of Pediatrics ( there was a RCT of 18 kids (I know is a small number, but this is randomized human data rather than rat studies). One group received 20 ml/kg bolus with correction of dehydration over 24 hrs. The second group received a 10 ml/kg bolus and correction of dehydration over a 48 hr period. The results showed no difference in MRI cerebral edema parameters at different treatment stages between the rapid fluid replacement approach compared with the slower infusion rates approach; and more importantly, MRI findings were consistent with vasogenic edema and were worse at the beginning of treatment compared with after-treatment in both groups. This suggests that sick DKA kids already have cerebral edema before initiation of therapy and edema improves after treatment independently of fluid infusion rates. Those who support the idea that rapid fluid infusion is the cause of cerebral edema in DKA treatment, say that it is due to rapid osmotic changes (we all have heard that), and there is probably some true about that. However, one important distinction to make here, is that osmotic cerebral edema and vasogenic cerebral edema are not the same. The TBI research ( that vasogenic cerebral edema is due to blood-brain barrier disruption resulting in extracellular water accumulation. In the other hand, osmotic cerebral edema is caused by osmotic imbalances between blood and brain tissue. These kids who got MRI early, all had vasogenic edema. How is that different by MRI? - I have no idea, but I am sure the radiologist have.

In regards to the factors that predict the development of cerebral edema, there is a great article from the NEJM from 2001, comparing 265 children with severe DKA. This study puts it all together very nicely. ( Some children developed cerebral edema and some did not. Analysis of other biochemical markers showed something very interesting. "Although osmotic factors and other mechanisms may play a part in the development of cerebral edema, our data lend support to the hypothesis that cerebral edema in children with diabetic ketoacidosis is related to brain ischemia. Both hypocapnia, which causes cerebral vasoconstriction, and extreme dehydration would be expected to decrease perfusion of the brain. In addition, bicarbonate therapy causes central nervous system hypoxia in laboratory animals with diabetic ketoacidosis. Hyperglycemia superimposed on an ischemic insult increases the extent of neurologic damage, blood–brain barrier dysfunction, and edema formation. This interaction might help to explain the occurrence of neurologic damage in association with minor degrees of cerebral hypoperfusion. Blood–brain barrier dysfunction and vasogenic edema may occur several hours after an ischemic insult as a result of the release of vasoactive substances and mediators of inflammation. The occurrence of cerebral edema several hours after the initiation of therapy thus correlates well with the hypothesis that the basis of this complication is ischemia. Finally, the more frequent occurrence of cerebral edema in children than in adults may be explained in part by the fact that children's brains have higher oxygen requirements than adults' brains and are thus more susceptible to ischemia".

A good while ago, Canadians also found that low CO2 and high BUN had the strongest association with cerebral edema ( Again.. these are sick DKA kids. This was a case control study, after adjusting for variables, found not association between the occurrence of cerebral edema in DKA and treatment factors. The authors conclude that the presence of cerebral edema before treatment of DKA and the association with severity of illness suggest that prevention of DKA is the key to avoiding this devastating complication. 

Summarizing... Here are the strongest associations with their respective OR's, CI and P values

  • Initial BUN (per increase of 9 mg/dl): 1.8 (95% CI: 1.2-2.7); p value 0.008
  • Initial partial pressure of arterial carbon dioxide (per decrease of 7.8 mm Hg): 2.7 (95% CI: 1.4-5.1); p value 0.002
  • Treatment with bicarbonate: 4.2 (95% CI 1.5-12.1); p value 0.008 (Don't do it!)
  • Rate of increase of serum sodium concentration (per increase of 5.8 mmol/l/hr):0.6 (95% CI: 0.4 - 0.9); p value 0.01
- Cerebral edema in the setting of DKA is more related to the severity of the primary disease process rather than the rate of fluid treatment. The pathophysiology is complicated, but hypoperfusion leading to cerebral ischemia along with damage to the blood-brain barrier all result in vasogenic edema. 
- Pedi DKA in shock -> Treat shock !  Their brain needs perfusion. However, be cautious and don't flood this kids with fluids, just restore tissue perfusion. Some guidelines (mostly from the U.S.) suggest an initial bolus of 20 ml/kg is a reasonable start point in shocky kids, with the option to repeat if there is no improvement in hemodynamics. However, a maximum of 30-40 ml/kg in the first 4 hrs of treatment is recommended with early consideration of sepsis if no response. This is when being a good clinician is so important. 
- Don't give bicarbonate, don't give bicarbonate and don't give bicarbonate. Is that clear enough?
- Having a healthy skepticism and questioning the old dogmas may get us closer to the truth about what is the right thing to do. 

Saturday, December 7, 2013

Emergency Radiology and Pregnancy

My apologies for the delay in posting something new, but this topic required a lot more reading than initially expected. There is a lot of information from very diverse sources, not just medical imaging literature but also from genetics, physics and the energy industry as well. Very interesting stuff!

The pregnant patient is, and will always be, a complex patient. The presentation of life threatening diseases is often atypical, symptoms that could be part of a normal pregnancy may also indicate serious pathology, the physiology of pregnancy is different from a non-pregnant female and to make things even more complicated, there is a little human being inside! No wonder why the sick pregnant patient in the ED scares the socks out of us. We all use our clinical acumen but that is often not enough to decide sick-or-no-sick, and we must rely on imaging technology to aid in the diagnosis. There is handful of non-pregnancy related diagnoses that create all the problems and split hairs, these include appendicitis, renal colic, ovarian torsion, hemorrhagic ovarian cysts, pulmonary embolism and trauma. It is well known that whenever possible, ultrasound is the modality of choice when it comes to imaging the pregnant patient; unfortunately, it is not always conclusive and CT scan becomes the better choice. That's when the "radiation talk" should take place. I have heard all kind of crazy things about this, mostly due to lack of information in patients and even providers. Therefore, I would like to cover some basic physics about radiation and its effects, just to put things in perspective.  It will not make you a physicist, but you can sound like one when talking to the radiologist, and that's very useful. Shall we...?

Fact number 1: Radiation comes from everywhere and everything; from natural sources like air, water, food, plants, ground and cosmic; as well as artificial sources like the electronics we use everyday, buildings, occupational exposures, nuclear and medical imaging, etc.

Fact number 2: There are several units to measure radiation. Depending on which system is used in the country you live in, there are Rads/Grays and Rems/Sieverts. 1 Rad = 1/100 Gray and 1 Rem = 1/100 Sievert. For the purpose of this review, it is worth remembering Grays and Sieverts. A Gray (Gy) is a measure of absorbed ionizing radiation which is equal to 1 Joule of energy release in 1 kg of mater. A Sievert (Sv) is the unit of the effective dose of radiation that has a biological effect on tissue, 1 Sv is equal to effect of 1 Gy over the exposed tissues multiplied by the specific weighting factor. If this sounds too complex (and believe me, IT IS) just remember that a Gray is the amount of radiation received by the tissues and a Sievert is the unit for the effects of 1 Gray of radiation in humans. Although technically are not the same, for practical purpose they can be thought as similar units.

Fact number 3: The average dose of background radiation a human accumulates just for being temporary habitant of this planet is somewhere between 2 and 7 mSv (mili-Sieverts) depending on location and altitude. There are high radiation locations in areas of nuclear disasters, natural occurring "leaks" from the earth, mines and high altitude.

Fact number 4: From the different types or radiation, ionizing radiation is the one used in medicine. Its ability to pass through tissues of different densities makes it ideal for imaging technology and treatment of cancers. The problem is that as it goes through to the tissues, it deposits enough energy to brake molecular bonds and displace electrons from atoms creating free ions (therefore the name ionizing); this results in damaged bonds in the DNA of living cells.

Fact number 5: In industrialized countries, the most common sources of artificial source of ionizing radiation is medical imaging with an average of 3 mSv per year per person (world's average is 0.6 mSv) and air travel with 2.1 mSv per year. Of note, heavy smoking (1 pack per day) results in radiation dose of ~160 mSv per year directly into the lungs! (If you smoke, you need to stop)

Well... I think that's enough physics for one day! Now let's apply these facts to the medical imaging in humans, including unborn babies.

We just learned about the effects of ionizing radiation in living cells and that we all are exposed to radiation from multiple sources at any given time. Then why aren't we all dropping death with cancers of all types? - Well, that is because there is an extremely sophisticated and highly specialized enzymatic complex system that detects, repairs or destroys damaged cells. This awesome system corrects billions of DNA mishaps a day and maintains cellular functions. Ionizing radiation in high doses, and specially after repetitive exposure, can eventually overwhelm this mechanism and lead to various types of malignancies. The fast mitotic fetal cells are particularly vulnerable to these effects from radiation, therefore is a good idea to limit fetal exposure whenever possible.

I found this table with the average dose of radiation from different studies, their equivalent to background radiation in years and its risk for malignancy

Too much is said about the fetal radiation risks for various types of imaging technologies derived from phantom models, animal and human observational studies; all thrown in the same bowl with extrapolated nuclear bomb survivors and nuclear disasters data. The result is an estimation of risk, but let's be clear about something... No one has solid, indisputable human information with a dosimeter next to a developing fetus to accurately measure radiation doses in-utero and its effects based on randomized studies (and we never will). All of the current available recommendations are predicated on estimated risks based on less-than-perfect data. Having said that, this is all we have and it seems to be enough to draw some conclusions.

The background dose of radiation for 9 months of pregnancy is estimated at 0.5 to 1 mGy, and the threshold for increased risk of fetal anomalies or pregnancy loss is 50 mGy (5 Rads) or 50 mSv (5 Rems). Standard radiological tests produce radiation doses far below the 50 mSv threshold. The aggregate risk for spontaneous miscarriage, major malformation, mental retardation and childhood malignancy in the general population is estimated to be about 28.6%. A dose of 50 mSv of ionizing radiation will increase this risk to approximately 28.8%. Specifically about childhood cancer, defined as any cancer with onset before age 15, the most common being leukemia, the average risk of leukemia in general pediatric population is about 0.036% (3.6 per 10,000), exposure to 50 mSv will increase this risk to approximately 0.06% (6 in 10,000).  From these statistical models we can conclude that although the risk of negative effects of the cut off of 50 mSv is not zero, it is indeed, very very small. The National Council on Radiation Protection and Measurements, and the American College of Obstetricians and Gynecologists have both agreed that the potential health risks to a fetus are not significantly increased from most standard medical tests. The American College of Radiology (ACR) has also come on record saying that "No single diagnostic procedure results in a radiation dose that threatens the well-being of the developing embryo and fetus" (Hall EJ. Scientific view of low level radiation risks. Radiographics. 1991;11:509)

This table shows the fetal dose of common radiologic tests. All these give less than 50 mSv, so it is safe to say that when we need to image a pregnant patient using ionizing radiation, we can proceed knowing that any of the studies we use in the ED represent low risk.

This next table summarizes the average dose of multiple radiologic studies and the number of studies needed to reach the aggregate dose of 5 Rads (50 mGy/mSv)

And this last table is from the ACR 2013 revision of its practice guideline on imaging the pregnant or potentially pregnant women using ionizing radiation, reaffirms what has been said by other organizations regarding the cut off of 50 mGv as safe level. 

What about contrast? - Well, I did find some useful information about that from the ACR 2013 manual on contras media. Basically it says that the water soluble iodinated low-osmolarity contrast media (the one use currently) does cross the placenta but there is no current evidence of mutagenic or teratogenic effects from it. As far as the effect on neonatal thyroid function, the document says that the amount of contrast in the fetal circulation is small and transient, and there are no reported cases of neonatal hypothyroidism in babies whose mothers received this type of contrast and the FDA has given it category B status. The ACR's recommendation about the Gadolinium-based contrast media (GBCM) used in nuclear medicine studies is not as strong. It says that although there have been no know adverse effects to human fetuses by the use of this agent, there is only one study of 26 pregnant patients who were exposed to Gadolinium during the first trimester, none had teratogenic nor mutagenic effects of the progeny. Therefore, the use of GBCM should only be used when the benefits justify the potential risk to the fetus. 

OK... are you with me so far? - Good! Let's now get practical and put all this theory where the rubber meets the road, at the bedside of the pregnant patient with a potentially serious diagnosis.

Let's start with the rule-out appendicitis case and the ultrasound comes back with something like this "Appendix not seen, acute appendicitis cannot be excluded, consider pelvic pathology... clinical correlation required". Now what? - Sure, you can try to put your pregnant patient in the MRI for 30 minutes and hope for a clear diagnosis; however, MRI is not as sensitive nor specific compared with CT, thus resulting in equivocal results, and most radiologist are far better diagnosing acute appendicitis on CT than MRI. CT with oral and IV contrast is the better choice, and the 25 mSv dose of radiation are still considered relatively safe by ACR and ACOG. Now the conversation with the patient should include the following... If this is acute appendicitis and we don't find out on time and it ruptures, there is between 6-37% chance for fetal loss, maternal morbidity and mortality range around the 5% and 1% respectively. and the risk of the radiation dose of the CT abd/pelvis for anomalies, fetal loss or childhood cancer is less than 1%. It seems clear that scanning is the best option. 

Urolithiasis with renal colic is the most common non-obstetric diagnosis requiring hospitalization, affects about 1 in 1500 pregnant patients and it is often confused with appendicitis, diverticulitis, ovarian pathology and placental abruption. Ultrasound is first line test to diagnose urolithiasis during pregnancy. When the stone is visualized that's great, but when all you see is hydronephrosis it is hard to tell if that is the hydronephrosis of pregnancy or due to a distal obstruction. The good news is that about 60-80% of stones will pass with conservative management, the bad news is that 20-40% will not and urologist use size of stone and location to determine treatment options. MRI is good to see hydronephrosis but not so much stones, so it doesn't really have significant advantage over ultrasound. Intravenous pyelogram has fallen out of favor because of the 50% higher radiation dose compared with CT scan and it only provides imaging of the urinary tract. CT scan again comes as top option for complicated cases of urolithiasis because of its high sensitivity and specificity, and ability to screen for other intra abdominal/pelvic pathology. 

The pelvic pathology including ovarian torsion, adnexal mass, hemorrhagic cyst and degenerating fibroid are best seen with ultrasound, so no surprises here. However, in late pregnancy the gravid uterus may obscure adequate view with the ultrasound. The MRI without contrast could be used in the stable patient. CT with IV contrast becomes the imaging modality of choice in the unstable patient with hemoperitoneum.

Pulmonary embolism is, on it self, a monster topic which becomes even more monstrous in the pregnant patient. With a mortality approaching 15% and significant morbidity of anticoagulation, we must get this right in a timely fashion. There are several protocols including trimester adjusted D-dimer + leg ultrasound in leu of pulmonary imaging. In patient with symptoms suggesting PE and (+) US for DVT, most will go ahead and treat; but when this approach is not diagnostic, pulmonary imaging becomes mandatory and the options are CT pulmonary angiography (CTPA) vs V/Q scan. The ACR rates both studies as adequate in the pregnant patient with radiation doses below the 50 mSv limit. The American Thoracic Society in its 2011 practice guidelines recommends plain chest x-ray as the initial radiation-associated step. If the CXR is normal, proceed with the perfusion phase of V/Q scan followed by the ventilation portion if abnormal. If CXR is abnormal, then CTPA is recommended. The algorithm looks like this...

The problem with this approach is that if the V/Q is inadequate or non-diagnostic (and many of them are), then you still have to proceed with CTPA. The advantages of CTPA is that it can also provide alternative diagnosis (i.e. pneumonia) and is more widely available compared with a V/Q scan. The fetal radiation doses of both studies is fairly comparable with an average of 0.2 mSv for CTPA, 0.12 for the perfusion-only V/Q and 0.2 for the ventilation portion of the V/Q scan. The remaining issue to discuss about CTPA is the radiation exposure to the hyperplastic breast tissue of the pregnant patient, which is said to increase life time risk for breast cancer in about 1%. Breast shields and timed beam techniques can significantly lessen this exposure.

The final diagnostic dilemma to review is trauma. This is the easy one because everyone agrees that when it comes to radiology studies, you just do it. Trauma is the number 1 reason for non-obstetric mortality during pregnancy, and unless you are ready to do a perimortal c-section, treating mom is the best way to treat baby. The pregnant trauma victim should be imaged just as the non-pregnant with x-rays, CT or angiography when required. Sure, you take a quick look with the US to check on the fetus and the placenta, but don't get hang on that screen while the mom is bleeding out, and remember that every pregnant trauma victim beyond 24 wks gestation once stable, should be placed in continuos cardio-tocographic, which is the most sensitive way to diagnose placental abruption. It is possible that mom may require multiple studies that may add up radiation doses of > 50 mSv and rarely > 150 mSv, and someone needs to keep track of what studies have been done and what studies are still needed. In such cases with high fetal exposure doses, therapeutic abortion should be discussed with the patient.

Wow... you are still reading! I am sorry this topic is too long, but I think it contains useful information that can be applied anytime when you pick up a chart saying "20 wk pregnant with abdominal pain". Now, it is time for final points.

Pregnancy test. The ACR says that for negligible risk examinations like CXR or extremity plain films, pregnancy test is unnecessary. Documentation; when higher risk examination is needed make sure to document clearly and completely. Tell the chart you have discussed alternative diagnostic options with the patient, mention the risks of doing and not doing the test, and what you feel is in the best interest of mother and baby. Finally, remember that avoiding radiologic tests in a potentially life threatening condition in oder to avoid fetal exposure to ionizing radiation is not going to score you any points when you end up with a dead mother, so do what it right for your patients.