Approach to the Fussy Infant

There are many different types of challenging patients that we all dread seeing when they pop up on the board. Whether the patient’s chief complaint is headache, back pain, or pregnant female with abdominal pain. Another very challenging patient presentation is the crying infant. The differential when evaluating a crying infant is broad. In this post I will include a list of differential diagnosis to consider based on organ system and then a patient I had that presented in this way.

CNS- Meningitis, epidural hematoma, subdural hematoma, hydrocephalus

HEENT- Skull fracture (accidental or non- accidental trauma), ocular foreign body, corneal abrasion, otitis media, nasal foreign body.

Cardiovascular- SVT, myocarditis, congestive heart failure

Pulmonary- foreign body in airway, bronchiolitis, pneumonia

GI- Malrotation/volvulus, pyloric stenosis, appendicitis, gastro-esophageal reflux, intussusceptions, anal fissure

GU- Testicular torsion, UTI, incarcerated inguinal hernia, soap vaginitis, phimosis, paraphimosis

Musculoskeletal- Fracture, septic arthritis, dislocation, hair tourniquet

My patient presented as a 1 month old male with his Spanish speaking Hispanic parents. Mom stated that he has been crying consistently for the past 4 days. She does not remember a specific time when the crying started but she states it has not improved.

Mom is breastfeeding the baby and denies any dietary changes. The baby was full term and mom had no complications with the pregnancy. Patient up to date on all vaccinations. Baby has been afebrile and per mom has not been lethargic. Baby is still feeding well and gaining weight appropriately and mom denies any projectile vomiting after feeds, denies any change in stooling, and notes good urine output. Baby lives at home with mom and dad and I have no red flags to suspect non-accidental trauma.

On exam he is overall well-appearing and does not appear to be in any type of distress: crying but consolable. He appeared to be healthy. He was interactive, tracking me with his eye movements, and did not appear to be meningitic or lethargic. Heart and lungs were unremarkable and abdomen was soft, nontender and non distended. GU exam (make sure you do this) was unremarkable. Baby was moving all extremities while lying on the oversized adult bed in the middle of the hallway and on inital exam did not appear to have any outward bruising or signs of trauma.

Upon removing the patient’s socks I noticed something odd on his second toe of his right foot. Just distal to his PIP joint he had a circumferential red line. As soon as I started to examine that toe his crying increased substantially. On further examination he had a hair tourniquet that had eroded its way all the way down to the bone of the middle phalanx of the second toe.

At this point the baby was still in the hallway and we took him to Room 9 to attempt to try any remove it. I am sure you can imagine how awesome this was on a crying kicking 1 month old. We attempted to unwind the hair but ultimately were unable to do so as it was just to deep into the tissue. I called Kosair and the patient was transferred and I do not yet follow up on the final outcome.

This just re-enforces the importance of a good head to ahem, toe physical exam on patient’s that are not straight forward. Mom had been with the infant 24/7 for the past 4 days and had not noticed this; not to mention who knows when the hair tourniquet actually started. Just something to keep in mind and hopefully this helps next time you all have to examine a crying baby.

 

Activating a Level I from EXI

Presentation: late-20s male, denied any medical history, presented after he got hit multiple times in the head with a two-by-four when he drunkenly stumbled into a stranger’s yard while walking home.  He had some abrasions to the head and face, and was obviously intoxicated, but had normal vitals and a nonfocal neurologic exam.  He had no visible trauma to the extremities or torso on initial evaluation and had reportedly been ambulatory at the scene.  He was cooperative and really wasn’t causing too much trouble for an EXI patient on whatever night it was.  So I went with the “liter of fluids, basic labs, scan his head and c-spine, and watch him while he sobers up” approach.  It’s one I’ve used many times before and since, and one that in all honesty I still stand by for this patient, at least initially.

Fast forward a handful of hours, his scans are negative, and he’s sobered up nicely.  He’s still cooperative, but having a little bit of left side pain.  He wasn’t very hungry but had taken a few sips and tolerated them okay.  So our fabulous nurse and tech tell me he’s “walky-talky” and probably going to be ready to go soon.  I start to get his discharge ready, when they catch my eye and call me over.

What I see when I get over there is not at all what I expect based on my last spin through EXI on my way out of Room 9…

Now, this guy looks sick.  Legitimately sick.  Not just unsteady or a little too drunk to walk, he is GHOSTLY pale and unable to stand.  He’s got a pained grimace on his face and is about to pass out.  We got him back into his chair and someone went off to grab an extra bag of fluids and the ultrasound for me, since his heart rate had spiked up to 125.  After he was flat in his chair, I threw the ultrasound probe on his abdomen: RUQ was equivocal, but his LUQ had a nice huge stripe of free fluid.  He also had some new ecchymosis in his left lateral abdomen/LUQ.  Unfortunately I was in a little bit of panic mode and didn’t save his ultrasound images, but it was crystal clear to me what had happened: something had been bleeding for a while and was now causing a big problem.  So we rolled his chair into Room 9, plopped him onto a bed, and hit the Level I button when his manual systolic pressure came out at 85.  We pumped fluids in him and got blood to the bedside and into his veins right about the same time the wedge and chief showed up.  He stabilized enough for the scanner after initial resuscitation, and Trauma stood by in radiology to watch the images come up.

His spleen was pretty much ripped in two.  He didn’t appear to have any active extravasation (surprisingly, as far as I recall), and his pressure was improving though his heart rate wouldn’t go below 100 for more than a few seconds at a time.  I talked to him, I talked to his mother, and I talked to the Trauma folks.  We had enough time to get repeat blood work, discuss the impending surgery, and get him packaged up as stable as he was going to be before they whisked him away to Room 4 (or maybe 6, whichever).

He recovered uneventfully from his splenectomy, and was discharged from the hospital a few days later.  He had the best possible outcome given the particulars of his eventful time in the ER.  But I kept asking myself a handful of questions over the following days that I still think about from time to time.  What if we had walked him earlier, well before his hemorrhage was on the border of Class II and Class III?  Could he have gone home and died of hemorrhagic shock from a missed spleen injury?  What if I had scanned him earlier and he had only had a tiny contained rupture with no extravasation?  Would he have ended up in OR 4 anyway but gone there from the floor or PCU instead of from the ED?  How should I have proceeded differently?

After kicking myself for a couple of days, I talked with the attending who had been on with me at the time all of the kerfuffle went down, and felt much better about my decision-making process.  I distinctly remember him having no torso trauma or pain on my first assessment.  Man scanning this young, otherwise healthy patient was not indicated.  It was not contraindicated, but would have seemed superfluous and a misuse of resources based on his initial presentation.  As a side note, which was honestly extremely relieving to me, Trauma wasn’t all that critical of my decision-making process and was just glad we caught it before it got any worse.

In doing a little bit of background research, it appears that delayed spleen rupture is a not-entirely-unheard-of entity, but is debated in some surgical literature as a term coined as an alternative way to describe a missed initial diagnosis.  Regardless of what it’s called, it does happen.  Though, when it does, it’s usually after at least a couple of days (sometimes even a week), not just a few hours.  The literature focuses more on whether it’s a legitimate problem than how to manage, as the management is no different from a normal spleen rupture.  Operative intervention is the usual course, though some small lacerations/subcapsular hematomas are electively managed with observation first, especially in high-operative-risk patients.

My experience gave me 3 lessons to take away.

First: Young, healthy, adult patients can trick you just like children, with vitals not markedly abnormal until a big problem is present.  So you need to reassess them.  I know I’m as guilty as the next person of not always reassessing as thoroughly as I’d like, especially on a busy shift, but I’m also much more aware of who will need me to do a little more work before I can bless their departure.

Second: Drunk (or otherwise intoxicated patients) can trick you and hide serious problems.  Be aware of this going forward, because it doesn’t mean you need to man scan everyone, it just means you need to keep your mind open to injuries that aren’t initially apparent.

Third: Adjusting the plan and course is entirely okay, and in some ways it’s what EM is built for.  It’s why we get gaits on traumas with leg pain.  It’s why we walk our drunks and PO challenge our vomiting patients.  And it’s something we have to keep in mind because we’ve all seen patients who went from apparently fine to nearly-dead in what seemed like a single instant.

Another abdominal pain

I had a patient in her 30s that presented with 1 day hx of N/V and diffuse abdominal pain that was most severe in her epigastric and LUQ and radiated to her back.  She had PO intolerance since the pain started the night before. Past medical hx was significant for R nephrectomy that she states is because her “kidney wasn’t working right”. Pt says that this pain feels just like the pain she had from that kidney.

PE: VSS, afebrile. She is curled in the fetal position and yells anywhere you touch on her abdomen but states that the worst pain is when I press her epigastrum and LUQ. She has a large RUQ scar from her nephrectomy. No CVA ttp, negative murphy sign.

At this time my differential included pancreatitis vs PUD vs gastritis vs pyelonephritis
Labs come back with lipase wnl, no WBC, UA with a lot of epithelial cells and a few WBC. Acute abdominal series xray is wnl

I reassess patient after dilaudid and zofran and she states nausea has resolved but still has severe epigastric/LUQ pain. On reexamination the rest of the abdomen is nontender. The amount of pain she is experiencing in her epigastrum/LUQ concerns me and its not pancreatitis based on the lipase so I order a CT abd/pelvis and I put in the ordering comments “diffuse abdominal pain most severe in epigastric and LUQ”.

The radiologist walks over to the department to tell me that the patient has appendicitis and her appendix which is thickened and with fat stranding is in the mid right abdomen instead of RLQ hence the atypical location of her pain. My assumption is that the reason her appendix is so high is from scar tissue secondary to her transabdominal nephrectomy.

I post this to remind everyone that while the RLQ is the most specific place to have pain from appendicitis, the pain can be anywhere (previous abdominal surgery (in this case), retrocecal/pregnancy, etc).

Just get a walking O2 sat

In patients with some suspicion for PE, even with a negative d dimer, I have often ordered a walking O2 sat and HR. This was not really evidence based, but maybe now could be. Below is the abstract for a prospective cohort study of patients known to be with and without PE. Interesting data even if only 114 patients. Cannot get full text yet.

Take home point. Combined sensitivity of HR increase of 10 BPM AND Sat decreased of >/= 2% was 100%.

ie if HR does not go up by 10 or more AND sat does not drop by 2 or more they are very unlikely, based on this small study, to have a PE.

 

 

CJEM. 2015 May;17(3):270-8. doi: 10.1017/cem.2014.45.

Ambulatory vital signs in the workup of pulmonary embolism using a standardized 3-minute walk test.

Abstract

OBJECTIVE:

Diagnosing pulmonary embolism can be difficult given its highly variable clinical presentation. Our objective was to determine whether a decrease in oxygen saturation or an increase in heart rate while ambulating could be used as an objective tool in the diagnosis of pulmonaryembolism.

METHODS:

This was a two-site tertiary-care-centre prospective cohort study that enrolled adult emergency department or thrombosis clinic patients with suspected or newly confirmed pulmonary embolism. Patients were asked to participate in a standardized 3-minute walk test, which assessedambulatory heart rate and ambulatory oxygen saturation. The primary outcome was pulmonary embolism.

RESULTS:

We enrolled 114 patients, including 30 with pulmonary embolism (26.3%). A ≥2% absolute decrease in ambulatory oxygen saturation and an ambulatory change in heart rate >10 beats per minute (BPM) were significantly associated with pulmonary embolism. An ambulatory heart rate change of >10 BPM had a sensitivity of 96.6% (95% confidence interval [CI] 83.3 to 99.4) and a specificity of 31.0% (95% CI 22.1 to 45.0) forpulmonary embolism. A ≥2% absolute decrease ambulatory oxygen saturation had a sensitivity of 80.2% (95% CI 62.7 to 90.5) and a specificity of 39.3% (95% CI 29.5 to 50.0) for pulmonary embolism. The combination of both variables yielded a sensitivity of 100.0% (95% CI 87.0 to 100.0) and a specificity of 11.0% (95% CI 6.6 to 21.0).

CONCLUSION:

In summary, our study found that an ambulatory heart rate change of >10 BPM or a ≥2% absolute decrease in ambulatory oxygen saturation from baseline during a standardized 3-minute walk test are highly correlated with pulmonary embolism. Although the findings appear promising, neither of these variables can currently be recommended as a screening tool for pulmonary embolism until larger prospective studies examine their performance either alone or with pre-existing rules.