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One our own Ophtho residents, Dr. Mark Mugavin (PGY-3), has started a YouTube channel where he is posting a series of Ophtho lectures as part of an education project. These lectures are designed for non-Ophtho residents who may run into eye complaints in their practice – AKA us.
So far he has 3 lectures posted, Ophthalmology ER, Pupils, and Practical Ophthalmology Trauma. I’ve watched them and found them helpful, would especially recommend them to the interns. Here’s the link to his channel:
A late 20s F G4P3003 at approximately 6 weeks gestation by LMP presents with a chief complaint of vaginal bleeding. A few hours PTA, patient states she felt a “gush of blood” with some mild abdominal cramping. VSS. On exam, noted to have a moderate amount of vaginal bleeding per the os. On our bedside ultrasound we note what appears to be a viable IUP with cardiac activity. However, the uterus appears septate, with half containing the IUP and the other half more hyperechoic/solid in nature. We were concerned for a possible subchorionic hemorrhage and consulted OB/GYN. Our bedside US image is below:
OB came down with their Cadillac ultrasound and confirmed our findings. For comparison, here is their much clearer image:
For this patient, with this large of a subchorionic bleed, the likelihood of her carrying this pregnancy to term was low. They planned to have her follow up in clinic for a repeat ultrasound in 2 weeks to reassess viability. Per our OB colleagues, other things on the differential included a fibroid. However, as this patient had 3 very healthy and rambunctious boys at the bedside with her, OB commented that a fibroid that large would likely have resulted in infertility.
And from UptoDate:
“A subchorionic hemorrhage or hematoma is a risk factor for spontaneous abortion, particularly when it amounts to 25 percent or more of the volume of the gestational sac. A meta-analysis of seven comparative studies found that women having a subchorionic hematoma had a significantly increased risk of spontaneous abortion, compared to women without such findings (18 versus 9 percent; OR 2.18, 95% CI 1.29–3.68). The findings also are associated with an increased risk of placental abruption (4 versus 1 percent; OR 5.71, 95% CI 3.91–8.33) and preterm premature rupture of membranes (4 versus 2 percent; OR 1.64, 95% CI 1.22–2.21). The increased risks of preterm labor and stillbirth appeared to be dependent upon the presence of vaginal bleeding.
Pregnancy outcome associated with subchorionic hematoma also relates to location, with worse outcomes observed for retroplacental hematomas, compared to marginal hematomas. The location, rather than the size, of a subchorionic hematoma may be the most important predictor of pregnancy outcome. Evidence relating to the size of the hematoma and the risk of adverse outcomes is inconclusive.
The only management option for subchorionic hematoma is expectant. There is insufficient evidence regarding whether bed rest decreases the risk of pregnancy loss when a subchorionic hematoma is present. Some clinicians repeat an ultrasound in one to two weeks to confirm fetal viability and assess any change in size of the hematoma, primarily to provide reassurance to the patient. A subchorionic hematoma is not an indication to conduct a diagnostic evaluation for an acquired or inherited thrombophilia.”
Hey guys, I was hoping to get your input on an interesting case I had at Kosair over the weekend.
16 yo F (6 ft, 150 lb…so basically an adult) with a PMH of depression, self injury, and prior suicide attempt presents after ingesting citalopram 40 mg x 90 pills (her prescription, just filled 2 days ago) and concerta 10 mg x 8-9 pills (her brother’s). Patient had been at a party the night before, admitted to EtOH. Parents found out about the party the morning of admission and they had a big fight, took away car keys, etc. Patient decides to retaliate by swallowing pills, doesn’t tell anyone. Parents find her altered about 10:30, at Kosair at 11:40. Best guess is ingestion occurred sometime around 9-9:30am. Had one seizure at home per family, and one en route per EMS. Generalized, tonic-clonic, brief.
Initial exam shows a drowsy but arousable patient. Answers orientation questions x3. Initial vitals show HR 147, BP 135/70, RR 25, 93% on some oxygen (can’t remember if NC or nonrebreather). Patient denies CP, palpitations, SOB, abd pain, N/V, weakness/numbness. 4mm, PERRL. MAE equally. Old self injury scars noted on wrists bilaterally. Exam otherwise unremarkable.
We start IVs, get her on a non-rebreather, get IV fluids going. Agree that charcoal seems like a bad idea with her mental status and seizures. Mom has shown up, and as we’re getting some additional history from her, respiratory is placing EKG leads. I’ve talked to poison control. Then, about 20 minutes into her stay, she seizes again. We bag her through the seizure, again generalized tonic-clonic, and just as we’re pushing 2 mg of IV Ativan she comes out of it. She appears post-ictal, but is maintaining her airway. We load her with Keppra, and as I glance at the monitor behind the attending’s head, I notice that her rhythm has changed and she looks like she’s got a wide QRS. We confirm she still has good pulses, still out of it mentally, and since she’s already connected to the EKG leads we grab one (time stamp 12:04):
By the time we get this printed off (!!!!) she appears to have spontaneously converted back to sinus on the monitor. But woah, holy wide QRS/long QT batman! As the attending and I are pouring over the first EKG we get another one immediately (time stamp 12:08):
Thankfully, the QRS appears to have normalized, but we’ve still got a loooong QT, one of the things poison control definitely told us to look out for. Having seen a few similar ingestions at University, I suggest it’s time for bicarb. The attending wants to confirm and we quickly call poison control back, they agree and suggest starting a bicarb gtt, with pH goal of 7.45-7.55. Now we look back at the monitor and she’s throwing a ton of PVCs, captured here on EKG #3 (time stamp 12:12):
At this point, we opt to push an amp of bicarb while we’re waiting for pharmacy to tube up the bicarb gtt. I have to say, we see it start to work pretty darn quickly. The PVCs slow down, and her rate really starts to head back towards normal. We get an iStat (shot me down when I suggested one earlier), and a few minutes after we’ve pushed the bicarb we get an initial pH of 7.15, pCO2 of 51.5, HCO3 of 18, BE -11, and AG of 21. Electrolytes were WNL. By this time we also know her pregnancy is negative, and her serum tox is negative, no acetaminophen/salicylates on board. At this point, we talk about intubation as the patient’s mental status is still waxing/waning and she’s breathing shallowly with brief periods of apnea, almost like an opiate overdose. Attending wants to hold off, so I go off to call the PICU resident…and end up having to hang up the conversation halfway through when he changes his mind.
So we intubate her (finally got a peds tube…in an adult), the bicarb gtt comes up from pharmacy, they’re cleaning the PICU bed her, the last EKG looks 1000x better, and all’s well that ends well (time stamp 13:08):
So I’m curious to see what your all’s suggestions/thoughts are on this case. Looking back at that first EKG, how would you classify it? We’ve got a wide complex, monomorphic tachycardia that to me looks like sustained V tach (with a pulse). The long QT doesn’t surprise me, but this rhythm does as you’d typically you’d worry about it devolving into Torsades, but that’s not what this is.
Looking back, things I would have done differently: get a temperature sooner/order a total CK (serotonin syndrome could have been a factor and we don’t have a recorded temp until she’d almost 2 hours into her stay, no one ever ordered a CK), intubate sooner, loading her with keppra when she hit the door after 2 witnessed seizures, maybe could have prevented the 3rd?
Also, if you’re curious, I found this “Toxicology Conundrum” on LITFL that specifically discusses citalopram overdose. Has some good info, citalopram is definitely one of the more potent SSRIs, and QT prolongation is dose dependent and can be seen after ingesting >600 mg (this chick took 3.6 GRAMS). Seizures are also fairly rare, only seen in 2-3% of cases.
Middle aged male transferred from an OSH, accepted by ENT for a mandible fracture.
The patient is incarcerated, and was involved in an “altercation” with other inmates. The incident occurred around 2PM; but he didn’t report any of his pain to the guards until 10PM. On arrival at the OSH he had multiple contusions to his face/head, lacerations over his hands, and obvious dental trauma. The patient was also complaining of chest pain – he stated that another inmate had slammed him in the chest with his knee. Despite his age, the patient has a history of previous MI in 2011, cathed at U of L with no stents placed. Takes a baby aspirin, no other meds and no other PMH.
At this point, the patient is about 10 hours out from the incident. Work-up at the OSH with the following: neg CT head and CXR. CT face with a mandible fracture. Labs notable for WBC 17.8, Hgb 14.3, platelet 373, normal coags, normal electrolytes, BUN/Cr 14.0/1.1. Total CK 213 (55-170 normal), troponin <0.012, CKMB 1.66 (0 – 3.38 normal), myoglobin 271.8 (0-121 normal). Tox screen negative. EKG is as follows:
His hand lacerations were repaired and he was started on Augmentin for a human bite. ENT accepted, and the patient was transferred to U of L, arriving about 6 AM. Dental was consulted on arrival and splinted his teeth. By 9 AM ENT had evaluated the patient and admitted him to the floor, planning for surgical intervention.
The patient was an ED floor hold, and around 2PM began complaining of worsening chest pain. ENT was paged and ordered an EKG and a set of cardiac enzymes, coming down to re-eval the patient. His EKG now looked like this:
Enzymes came back with CK total 5024, CKMB 303, and troponin 44.1. Cardiology was consulted and ordered a stat echo and started the patient on ACS protocol. The echo showed an EF of 30%, an akinetic mid/distal anferoseptum and an akinetic apex. Cards initially thought that this was consistent with stress cardiomyopathy in the setting of trauma, but couldn’t rule out cardiac ischemia due to direct cardiac trauma. They planned to treat medically and cath in the morning.
Throughout the evening, he developed worsening ST elevation in his lateral leads and his troponin continued to rise, up to 67.0 by midnight.
The on call cath attending at Jewish was consulted and by about 3AM the decision was made to transfer the patient to Jewish for a cath first thing in the morning.
Final result: 100% LAD occlusion, secondary to direct cardiac trauma.
Definitely rare injury, but one to keep in the back of your mind, especially as it can occur in previously healthy, relatively young patients. Of note, these can have delayed presentations, up to several days. Typically occur after MVA, but there are several cases reports occurring after crush injuries, being hit in the chest by a soccer/rugby ball, and my personal favorite, one listed as “struck in the chest by an umbrella tip.”