Showing posts with label For My Own Edification (FMOE). Show all posts
Showing posts with label For My Own Edification (FMOE). Show all posts

1.15.2009

FMOE: Toxicology Case Answers

Case 1. 21 year old genius shows up in the ED. His girlfriend is concerned because he seems weak, acts like he's drunk, and is unsteady on his feet as well as slow in his responses. She is holding a plastic bag with what smells like model glue in it. Afebrile, RR 23, HR 80, BP 120/68.

1. What chemical element was this genius probably exposed to, given the odor?

Toluene is desired by high-seekers for its rapid CNS absorption and quick high; the toxicity here is obtundation, which usually clears quickly. Chronic users kill brain cells and become demented. Hydrocarbon ingestions typically damage the lungs more, but toluene goes straight for the CNS.

2. What secondary disturbance is likely causing his symptoms, especially the weakness?

Toluene can simulate a renal tubular acidosis and lead to hypokalemia and hypophosphatemia.

Case 2. A 25 year old sportsman was golfing when he felt a prick in his finger with some scant bleeding after searching for his golf ball in long grass. He finished the round, and now has increasing pain and swelling in his hand. He is starting to feel a bit weak. Temp 99.5, BP 85/50; right hand is tender, swollen, and bruised.

1. What happened? What are you worried about next?

This case best fits the effects of a snake bite; rattlesnakes are most common, and local tissue necrosis is common to most varieties. Some rattler varieties, specifically the Mojave rattler, will cause neurotoxicity, but only in the SW US, where you also find plague, hantavirus, and various other sundry complaints like coccidiodomycosis.

2. What is the treatment?

Crofab, so named because it affects crotalid venom, the main genus of snakes in the US.

Case 3. A 4 year old girl is brought to the ED by her worried grandmother (mothers always let grandma take over these days). She has not been her self; she is sleepy, and vomited once earlier. She found an empty bottle in the girl's room. She gives it to you; it smells like Icy Hot (NO USING GOOGLE!) There isn't a label. Temp 38.2, HR 130, RR 36. Exam reveals a drowsy, slightly diaphoretic child, with coarse rhonchi bilaterally.

Basic labs: sodium 142, chloride 104, potassium 3.4, bicarb 15, glucose 78, creatinine 0.8, BUN 12.

1. What did the kid drink?

Although med students all know that aspirin overdose gives a classic metabolic picture, I didn't know until I smelled oil of wintergreen that the oil is chock full of salicylates. In fact if you look it up on wikipedia, it's the main ingredient. So don't keep it in your medicine cabinet where your kids can get to it.

2. Med students, what is the disturbance seen in the labs and vitals? What can you do to treat her?

Med Students will be able to tell you better, but salicylates create a mixed metabolic acidosis and respiratory alkalosis through direct stimulation of central breathing centers beyond physiologic compensation. There's some computations to do...maybe later. As far as treatment, you can start patients on a bicarbonate drip to alkalinize the urine and trap the acid in an ionic form. ASA is also dialyzable.

Case 4. Three sixteen and seventeen year old males (automatic geniuses, I was never stupid when I was that age) arrive in the ED, combative, mumbling, and completely incoherent. Found by the fuzz drinking funky tea. A representative exam on genius 1, temp 102.5, HR 140, BP 140/70; agitated, small pupils, with red, warm, dry skin.

1. What is the toxidrome (for non-medical readers, mostly my parents, a recognizable set of symptoms that identify a specific toxin)?

This is a classic case of jimson weed ingestion. This plant, believe it or not, grows all over the US and, when boiled, is a mild hallucinogen and a strong anticholinergic. The toxidrome is dry, flushed skin, tachycardia, dry mucous membranes, fever, slurred speech, hallucinations, tiny pupils, urinary retention, consipation.

2. What is the antidote? When you would you use it? When would you NOT use it? What else can you give them?

Physostigmine is a direct cholinesterase inhibitor, thus increasing the level of acetylcholine and reversing the 'anti' choliergic effects. It does, however, prolong the QT interval and precipitate VT, I think, in cases of TCA overdose, a class which has anticholinergic effects. So, in a kid who got into the cabinet, it's not a good choice unless you like coding little kids. You can also use benzodiazepines and bicarb. I'll have to look up why bicarb works.

Case 5. 3 year old Max is brought in by his father reeking of garlic, vomiting garlic, and not acting like his usual self. Temp 37.4, HR 145 and regular, RR 42. Hyperactive bowel sounds, coarse rhonchi, constricted pupils.

1. What did Max ingest? Why is it not illegal?

The garlic odor is characteristic of carbamate insecticides which reversibly bind to cholinesterase and cause the opposite of jimson weed--or DUMBBELS, defacation, urination, miosis, bronchorrhea, bradycardia, CNS excitement, lacrimation, salivation. Atropine works (see below), and so does benadryl in large doses theoretically. The other toxins in this class are organophospate insecticides, which are irreversible but take time to convert, and Sarin gas, which is irreversible and converts almost right away. I think these should be illegal. They're poison.

What is the treatment? Hint: he should talk to the geniuses above and get some of their tea.

1.13.2009

Electrolyte Emergencies


The Cancun congress on EM had a great lecture available for download on electrolyte emergencies. I had wanted to look at these when I was on medicine, but they had a, well, different approach that took forever. This is much more EM specific.

Hyperkalemia is the most dangerous abnormality; the most common cause is 'not', that is, a lab draw error, hemolysis with the draw, and so on. An EKG guides how we treat the patient, so the first step in a work-up is re-draw and get an EKG.

Causes: Not; renal failure with acidosis; drugs over weeks or months (ACEI and ARBs, NSAIDs; and cell death (burns, tumor lysis). There are other causes, but these are the big ones.

EKG changes: tall T, loss of P, QRS widening, PR lengthening, sine wave (um, bad).

Treatment: calcium is only used in an emergency, defined by a widened QRS on EKG. Calcium for QRS (calcium chloride, it's faster), 2 amps of d50 and 10 U insulin, bicarb if acidotic but only if acidotic, albuterol nebs, fluid if hypovolemic.

hypokalemia=prolonged QT with U waves.

hypokalemia=hypomagnesemia, and K always goes with mag. We must replete both. If you don't give mag the K will stay intravascular and be excreted. The deficit is always worse than you think.

So, if you give K, give mag. Treat with EKG changes.

Hyponatremic emergencies manifest as altered mental status. Causes include runners drinking too much, women more than men, X use with dancing all night--water intoxication and hyponatremia. The big worry with hyponatremia is seizures and the AMS; the big worry with repletion is central pontine myelinolysis, or the so called 'locked-in syndrome', which is truly awful. Never correct a patient with symptomatic hyponatremia faster than 0.5 an hour or 10-12 a day. Seizures with Na below 120, like 100 or 110; intial 3% NaCl MAX 200 cc total, start with 100 cc bolus over 10 minutes. Must be previously healthy. So, the gorked out nursing home resident on diuretics and who knows what else who comes in 'just not themselves' with a sodium of 118 should not get 3% NaCl. The 19-year-old clubbing person with an empty water bottle seizing at 5 am with a sodium of 105 should, in two boluses, as above.

See? Much easier than the old hypovolemic-euvolemic-hypervolemic triad just for sodium and so on for each electrolyte...see this post.

12.30.2008

FMOE: Toxicology Cases

Here are some tox cases, one or two liners with vitals and questions. Pipe up if you think you know the answer. Answers will be posted within a week or so. When we did these stations, they provided a scent in a bottle. I'll try and describe them for you.

Case 1. 21 year old genius shows up in the ED. His girlfriend is concerned because he seems weak, acts like he's drunk, and is unsteady on his feet as well as slow in his responses. She is holding a plastic bag with what smells like model glue in it. Afebrile, RR 23, HR 80, BP 120/68.

1. What chemical element was this genius probably exposed to, given the odor?

2. What secondary disturbance is likely causing his symptoms, especially the weakness?

Case 2. A 25 year old sportsman was golfing when he felt a prick in his finger with some scant bleeding after searching for his golf ball in long grass. He finished the round, and now has increasing pain and swelling in his hand. He is starting to feel a bit weak. Temp 99.5, BP 85/50; right hand is tender, swollen, and bruised.

1. What happened? What are you worried about next?

2. What is the treatment?

Case 3. A 4 year old girl is brought to the ED by her worried grandmother (mothers always let grandma take over these days). She has not been her self; she is sleepy, and vomited once earlier. She found an empty bottle in the girl's room. She gives it to you; it smells like Icy Hot (NO USING GOOGLE!) There isn't a label. Temp 38.2, HR 130, RR 36. Exam reveals a drowsy, slightly diaphoretic child, with coarse rhonchi bilaterally.

Basic labs: sodium 142, chloride 104, potassium 3.4, bicarb 15, glucose 78, creatinine 0.8, BUN 12.

1. What did the kid drink?

2. Med students, what is the disturbance seen in the labs and vitals? What can you do to treat her?

Case 4. Three sixteen and seventeen year old males (automatic geniuses, I was never stupid when I was that age) arrive in the ED, combative, mumbling, and completely incoherent. Found by the fuzz drinking funky tea. A representative exam on genius 1, temp 102.5, HR 140, BP 140/70; agitated, small pupils, with red, warm, dry skin.

1. What is the toxidrome (for non-medical readers, mostly my parents, a recognizable set of symptoms that identify a specific toxin)?

2. What is the antidote? When you would you use it? When would you NOT use it? What else can you give them?

Case 5. 3 year old Max is brought in by his father reeking of garlic, vomiting garlic, and not acting like his usual self. Temp 37.4, HR 145 and regular, RR 42. Hyperactive bowel sounds, coarse rhonchi, constricted pupils.

1. What did Max ingest? Why is it not illegal?

What is the treatment? Hint: he should talk to the geniuses above and get some of their tea.

More next week, with the answers! I love my job!

11.26.2008

FMOE: Cope's Appendicitis

Ah, the appy. Every second-year med student can diagnose the acute onset of periumbilical pain that then localizes to the right lower quadrant. My first appy was a teenage girl who presented with pain, loss of appetite, fever, and dysuria for about twelve hours. Exam showed right lower quadrant tenderness. Labs were negative except for sterile pyuria. Even an obvious case like this one, where I walked out of the room and felt pretty sure, had a wrinkle, but sterile pyuria is a known associate, perhaps because the appendix can irritate either the ureter or the bladder.

But it's not until I read Cope that I look back on the appendicitis I missed in every single abdominal pain patient I've ever seen. Cope, incedentally, is the surgical bible of the acute abdomen. My surgery attending told us all to sit down and read it in a night, an 'easy read'. Perhaps, but to really absorb it...it's the book that keeps on giving. The following are some pearls to flesh out what we were taught in medical school.

History.

The 'march' of symptoms should be carefully sought, and is as follows: pain, followed by anorexia, nausea, or vomiting, followed by tenderness that is localizable but could be, according to Cope--and I love this--'somewhere in the abdomen or pelvis', followed by fever, followed by leukocytosis.

Put that in the context of what we think of as appendicitis. RLQ abdominal pain with a white count and fever. But a white count is the last finding. This march should be acute. Diagnosis of appendicitis should happen within 24 to 48 hours of onset, to avoid perforation. Fever first, nausea before pain, fifteen years of abdominal pain--these can make appendicitis less likely. Also, sudden onset of severe localizable pain, especially if it occurs in a 65-year old hypotensive veteran...perhaps not an appy.

Physical Exam.

This is the part of the reading that terrified me. The appendix can go anywhere in the abdominal cavity. Sweet. Frickin' awesome. I love that kind of a problem. If any localizable tenderness is found in the setting of a history that shows the above march, appendicitis should be on the list.

Of course McBurney's point must be palpated, and is perhaps the earliest localizable site of tenderness. Cope mentions light percussion as a very sensitive sign of parietal peritoneal irritation, which is what causes the tenderness--the switch from pain carried by the visceral peritoneal nerves to that carried by the parietal nerves. This can also cause hyperesthesia over the right lower quadrant to light touch. Test the psoas by rolling the patient to the left and extending the hip. Rovsing's sign is pain in the right with deep pressure on the left.

Perforation.

If the appendix does perforate, it can do so in a dizzying variety of ways. It can be localized or generalized, depending on whether it happens to be walled off or not. The most interesting difference, though, comes with rupture of an 'iliac' appendix versus the rupture of a 'pelvic' appendix.

The iliac appendix sits in the abdomen nestled against the pelvic girdle, while the pelvic appendix has dropped down behind the pelvic brim.

The iliac appendix should show a degree of guarding in the area we would expect, though, as in the case I started with, it can also produce urinary symptoms due to the proximity to the ureters. Overall, iliac appendiceal rupture should be found with a rudimentary exam of McBurney's point, which is reassuring since most people do that at least even when completing the intern's morning rounding exam (run in, stick stethoscope in the middle of the chest, push on tum, run out).

The pelvic appendix, though. Ah, the pelvic appendix. Much more terrifying. 'One of the most easily overlooked and therefore one of the most dangerous conditions that may occur in the abdomen'. Now that's saying a lot. A lot of badness can happen in one's abdomen. It's like a black box of poop-filled terror.

A perforated pelvic appendix may actually improve symptoms; the pain of distention is relieved (usually felt epigastrically) and the pus soup that was inside spills down deep in the pelvis, into the Pouch of Douglas.

So? SO, there will be little or no rigidity in the abdomen because the giant pus ball is in the pelvis. In fact, appendicitis can be misdiagnosed as PID, thereby lending insult--literally, if you're wrong and it's a young woman who is not sexually active--to injury. Things to watch for include pain with micturition, tenesmus, or diarrhea from inflammation. The cool maneuver here would be to rotate the hip internally to check for hypogastric pain, which would be wierd, right? Now, what if this is missed? It can go three or four days before the pus ball extends into the abdomen, and it tends to go to, wait for it, not the right, but the left side due to anatomy. Awesome.

See how I get paranoid? Now anyone who has abdominal pain in any location, with or without a fever, with our without nausea and vomiting, who may have diarrhea, pain with urination, pain with defacation, that has or has not been constant, probably has either early, late, missed, or atypical appendicitis and a giant collection of bacteria waiting to make them toxic and die.

This is how I think.

FMOE: The Apathetic Adrenal

4-yo female, african-american with big bushy pigtails and a vacant stare, presented to an outside hospital today after mom noticed that she was unresponsive. Initial exam notable for altered mental status, hypothermia to 35.2, decreased respirations, bradycardia. Her blood sugar was urecordable; she got glucagon IM by EMS, then more glucagon in the ED, then D25, then a dose of 20 mg hydrocortisone with subsequent return to baseline.

Mom is present with the child and notable for flat affect and a poor recollection of when she was seen last, by whom, or the name of any of the specialists that take care of her. She knows her PMD who is an NP at a free clinic.

Her past medical history is notable for a stroke at the age of 3 with persistent right lower extremity weakness and some speech delay, adrenal insufficiency of unknown etiology, and multiple seizure episodes accompanied by hypoglycemia.

The differential for shock that presents as above includes adrenal crisis but also sepsis and dehydration. The prodrome, if history is obtained, may often include a recent illness. This girl, g-tube dependent from her stroke, had vomited twice over the last two days and had generally been 'tired'. Check.

Physical exam findings may support CAH--abnormal genitalia, vitiglio, or the like, which I've never seen. She had no such findings.

The most interesting part of the case is, first, the appeal of a 'fix-it' intervention for a shocky patient--the hydrocortisone brought her back to baseline relatively quickly--and the oddity of such an apathetic parent and child. Their main question on rounds has been 'when can I go home?' A genogram reveals lots of hypoglycemia and stillbirths in first-degree relatives but mom didn't really care. I mean, I know you are a primary care giver for a sick kid and that can be tough but sheesh.

The other part of it is home management. Like asthma, if a kid with known AI starts to get sick, or get fatigued, parents should give them a stress dose of steroids--2 to 3 times their normal dose of supplemental meds. Mom HAD that at home. Although it's easy to use the retrospectoscope on her, it would've saved her kid a lot of possible harm to just treat early. And she's had a STROKE at the age of FOUR in the past! I would think that would catch her attention.

The other explanation is that she's very aware just tired of residents. That's possible.

Still, good to keep on the differential for a cold, slow, shocky kid, especially with a non-specific, malaise-and-angst-laden prodrome or some flu-like illness.

Photo Credit.

10.04.2008

FMOE: How To Not To Screw Up Headache Patients


Headaches are a very common complaint in the ED--3 to 5%--and only about 1% of those have a serious underlying cause such as meningitis, subarachnoid or intracranial hemorrhage, mass effect, carbon monoxide poisoning, or hypertensive encephalopathy, according to Rosen's, the bible of EM I'm working my way through.

This morning I had a oh crap in retrospect moment wondering if I missed something, so I'm going to use a case to illustrate how to go after this problem.

48-yo african-american female with hypertension, comes in with a BP of 202/104, a dull HA on the top of her head with no focal neurologic deficit for 2 days. How do I decide if this is a scary headache or not? My gut says not. So?

Red Flags:

1: sudden onset.

2. "The worst headache of my life."

3. altered mental status.

4. true meningismus. See this post for what 'true' means.

5. unexplained abnormal vital signs.

6. focal neurological deficits.

7. worsening under observation.

8. new onset of headache with exertion.

9. history of HIV.

She didn't have any of these, although the hypertension was a bit worrisome. Still, it's in her history so not 'unexplained'. So I have a textbook backing me up. That helps me avoid badness. Now, are there signs that she's all clear?

All Clear Signals:

1. previous identical headaches.

2. normal alertness and cognition for exam and for history.

3. normal neck exam. Our Brit attending does this well. Patient actively ranges chin to chest and looks up, looks side to side. Then, he supports the neck and asks the patient to go all floppy. He then gently but quickly turns the head side to side, for so-called 'jolt accentuation'.

4. normal vital signs.

5. normal or nonfocal neurologic exam.

6. improvement under observation.

The trick is that the patient gets flagged if they have any one of the red flags, and cleared only if they have all of the all clear signs, and she doesn't have normal vitals. So we observed this patient, and worked her up for hypertensive emergency--hypertension with evidence of end-organ damage by altered mental status, EKG changes, or elevated creatinine. Three hours later, after diltiazem, which she had not been taking for four days, and a gram of tylenol (which by the way is a wonder drug), she was better. Bye bye. The only thing bugging me was an EKG finding--she had mildly inverted T-waves in V4, V5, and V6 in the setting of left ventricular hypertrophy--enlargement of the heart due to the increased pressure it has to push against in the setting of hypertension. Why would that bug me? Because a web search of EKG findings in sub-arachnoid hemorrhage, the kind of headache I was worried about in her, showed inverted T-waves in V4, V5, and V6! Oh no, right?

Not really. This is like that 'true' meningismus or 'true' guarding. Inverted T-waves occur after major neurological events that should manifest themselves on exam, and are more impressive--see this example at a great ECG wiki site. Plus, these changes can even be seen during migraine headaches, a common and NOT life threatening presentation in the ED. Last but not least, the wiki site mentions deep T iversion in the precordial leads, i.e., V1 and V2, which correspond to the septum of the heart. This lady's EKG finding was in the leads corresponding to the anteriolateral portion.

So does LVH cause inverted T's? Sure does. See this link, first example. Phew. Fare well, nice headache lady. PLEASE take your diltiazem as instructed by your primary doc. Next time I might see inverted T's in you with altered mental status and severe, thunderclap headache, seeing as how you have hypertension too...sometimes I feel like I'm a pappa bird watching tiny little baby birds jump out of the nest when I discharge. I'll have to get over that, I suppose. Get jaded for my own protection. We'll see how it goes.

8.30.2008

FMOE, OB: Shoulder Dystocia

This is the second in a series called FMOE, which stands for For My Own Edification. Read on, but the post may be boring to anyone past an Intern, as I'm doing these to further my learning.

Coming off of OB, the next few will likely have something to do with pregnant women, who are total rock stars in my book, none more than my wife who has done things I would never have been able to do even if I had been born a woman. Too much of a wimp.

Shoulder dystocia (greek, dys for difficult plus tokos for birth) describes the failure of the shoulder to pass below the pubic symphysis during a spontaneous vaginal delivery with the head already delivered. In practical terms this is terrifying. The largest baby I delivered was 9 pounds, 12 ounces, and I had to pull like, a lot more than I expected to get her out despite excellent work by mom. It's scary when the baby feels stuck and you are hauling on its head. Normal deliveries require much more traction than you expect as a neophyte.

A truly stuck baby can have a severe shoulder injury or can asphyxiate and die. Badness, terrible badness. It's also hard to predict. If I had a 400 pound diabetic primigravid at post-dates in my ER delivering, I could say it's a good bet, but other than that, it can surprise anyone. What, oh what, to do?

Initial maneuvers. Of course, delivering the anterior shoulder requires a great deal of downward traction normally, so as a newbie, I have to remember to have may cardinal movements right; down for the anterior shoulder, up to the ceiling for the posterior. Simple suprapubic pressure from an assistant can help. The Gaskin Maneuver is mentioned on Wikipedia and via Google searches; the laboring mother is repositioned on all fours in order to create more space. I have not seen or heard of this maneuver in my EM textbooks or on the OB floors, but it makes great sense and should work--in a mother with no epidural! A Google search turns up anecdotal evidence, but this is no reason to disbelieve; midwives have been at their job a long time and much of OB is not evidence-based--try doing studies on pregnant women. Difficult.

Other initial options include the McRoberts maneuver, which is achieved by flexing and abducting both hips while laboring on the back. In practice, all deliveries were done in this position on the OB floor. If still stuck, the Woods Corkscrew maneuver is an option; reach in past the head with two fingers behind the stuck shoulder and rotate the baby about 180 degrees. Fingers go behind the shoulder to collapse the torso rather than open it up.

Truly horrible options then ensue. Keep in mind that by this time everyone is likely freaking out and the baby is probably quite literally dying in front of you. You can attempt to push the baby back into mom in order to go for a c-section--the so-called Zavanelli maneuver, which according to the namee was perfectly safe. This one is particularly funny since if you had such immediate access to any OB doc, you wouldn't be trying to push a large baby back into the uterus in the first place.

According to whonamedit.com, this maneuver was invented in the 70's by somebody named Gunn, and Zavanelli heard about it and told it to some other guy while he was volunteer teaching. So, if you want to use it, go ahead. Me, I'll put it in the same category as other things that should've stayed in the 70's, like the Pinto and Fleetwood Mac.

You can also deliver the posterior shoulder, by reaching up and grabbing the hand. Or, you can deliberately fracture the clavicle. Terrible sounding, but better than death. Actually, one of my deliveries had a fractured clavicle, and they heal well if there are no complications at the time.

The last option, a symphysiotomy, should scare everyone, not least because one of the tools needed is a finger guard. The pubic symphysis is the anterior joint of the pelvis and is just above the urethra and vagina. Apparently, in the late 1500's difficult deliveries were relieved with this method--using a scalpel to sever the ligament joining the two sides of the pelvis together anteriorally, allowing it to open so the baby can be delivered. I would have a hard time with this.

May we all have happy, quick but not too quick, ED deliveries, with no lacerations or post-partum hemorrhage.

Reichman and Simon, Emergency Medicine Procedures, McGraw-Hill

8.26.2008

FMOE: Obstetrical Bleeding, >20 Weeks

This entry is as much for me as for you, since I have to learn and retain information, and somehow putting it on a webpage helps.

So, a 18-yo (just so it's not too depressing, and she's 14) comes to the ED for sharp, constant pain just above the waist of her hipster jeans on the left that doubles her over and came on like a tornado on a midwestern summer night (sorry, can't give a canned case). No nausea, vomiting, or fever. She doesn't remember when her last period was, and she says she's not sexually active.

VS: 98.6, 54, 18, 80/50, 98% RA.

A brief physical exam reveals a rigid abdomen with guarding and rebound tenderness low in the left lower quadrant as awesome life-saving ER nurses place two large-bore IVs and run in liters of normal saline before she gets whisked off to the OR.

Not so common, probably too Grey's Anatomy-like, although if we were on TV then one of the residents would've just splashed betadine on her tummy and opened her up in the parking lot with the help of the nurse who's carrying the baby of her fiancee. Ectopic pregnancy can present as frank shock but is more likely to present unruptured, which means the differential for vaginal bleeding in pregnant women at less than 20 weeks gestation is simple: ectopic pregnancy or some permutation of a spontaneous abortion (threatened, inevitable, possibly missed). Less likely but possible choices include a molar pregnancy or a GU problem masquerading (UTI, pyelo, stone).

Overall, ectopic pregnancies are the second-leading cause of maternal demise in the US and complicate 2% of all pregnancies. For some reason the data is old but in 1986 that meant over 75,000 hospitalizations.

Medicine likes threes, and amenorrhea, abdominal pain, and vaginal bleeding is the ectopic triad but it's not very reliable--the patient may not be amenorrheic--at least not for the most typical six to twelve weeks--and may not be bleeding, at least not visibly. In the case above, the ruptured ectopic causes a bradycardic, hypovolemic picture due to the vagal stimulation caused by blood in the peritoneum. Not sure if it's real but I'm lookin' out for it.

Obviously, in the case above as in every female of child-bearing years plus five in either direction as well as drag queens a urine beta-hcg is the initial test usually done in the parking lot. A quantitative serum beta-hcg can be used but as Tintanelli's is very clear to point out (it's in bold for the idjits like me who skim) there is overlap and no level can reliably exclude an ectopic in favor of an IUP.

Ultrasound! Grand rounds last week, endovaginal U/S can find a gestational sack in the uterus at 5 weeks. Five weeks! That's barely long enough to start wondering and run to Walgreens, even if all our patients leveled with us and told us when they had last been sexually active or had a period.

Ectopic pregnancies can implant in the tubes most often, or interstitially in the uterine wall, or elsewhere; however, if there IS an EP, then the endometrial stripe should be thickened and without a gestational sac. That, along with the story, is likely enough to at least get an OB consult.

Treatment. In the above case, go directly to OR, do not pass GO, I would suppose. But most cases aren't like that. Options are laparoscopy which I would advise or IM methotrexate, which has a success rate quoted at 91%, but can cause a lot of pain as it aborts the EP chemically. The last 'detail' is to type and screen mom, and give her RhoGAM if she is Rh negative to prevent from alloimmunization.

Can't help but wonder how EPs are viewed by people who champion the rights of the unborn. If life begins at conception and this is an abortion would treatment of EPs be legal in the setting of a Roe v. Wade reversal that did not have an exception for the life or health of the mother? Hopefully they'll be smart enough to specify IUP abortions. I actually had a colleague in med school who was very strong in her views and said she would not offer methotrexate as it somehow was more abortion-y than laparascopy in this case.

Sorry for the boring post. I'm on medicine now, I don't have any good stories anyway. Besides, it's not all about you. Sheesh.