Please Tell Me What You Would've Done?

What do you think the patient's diagnosis will be?

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Rykielz

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I ran probably one of the strangest calls in my short 10-year EMS career today and I want some opinions on what could have been done differently and/or what your treatments would have been and why.

Story:

The call came in as a fall around 12:45 on a sunny day with no wind and an outside temperature of 61 degrees F. We arrived on scene and found a 52 y/o male c/o a near syncopal episode. The patient had been complaining of body chills, nausea/vomiting, and diarrhea for the past x3 days, but has not had a fever. The oral temperature he took last night was 98.1 F. The pt has had a non-productive cough for the same time frame. The patient states that he awoke this afternoon around 12:10 PM to urinate which he states was a regular amount and a light yellow color/transparent . The pt has been having diarrhea as well which he states is completely liquid and a light brown color. The patient had not yet had a bowel movement today and did not feel the urge to do so. The patient last vomited last night which consisted of the chicken noodle soup he ate earlier that evening. No blood was present in the urine, stool, or emesis. Pt states that after he went to the restroom he was walking down the stairs of his home and suddenly felt weak, lightheaded, dizzy, and his sight "went black," but he was able to hear and comprehend what was occurring and remembered the events as they transpired. These sensations lasted approximately 30 seconds according to the patient. The patient was assisted to the tile floor at the base of the stairs by his daughters, laid into a supine position, and 9-1-1 was called. We arrived about 15 minutes after the near syncopal event. Upon assessment the patient was A&O x4 with a GCS of 15 and denied loss of consciousness, pain of any kind, chest discomfort, dyspnea, dizziness, lightheadedness, blurred vision, headache, and nausea. No signs of trauma, JVD, or pedal edema were noted. The patient's only complaint while laying supine on the floor was general weakness and to give greater detail he stated, "it's hard for me to move my arms and legs." The patient had not taken his medication today, but has been taking it as prescribed. The patient went to bed yesterday evening around 10 PM, feeling nauseated and with an upset stomach after having vomited. The patient states that his bedroom is temperature regulated in "the high 60s" and he slept in thick blankets while wearing his full-body pajamas. The patient states that he has been vomiting 5-6 times a day with diarrhea episodes approximately 3-4 times a day since the onset of the symptoms x3 days ago. The patient states that he has been primarily on a liquid diet and has been drinking "G2 gatorade" to keep replenish the lost fluids. The patient also denied any recent drug or alcohol use. The patient also denied taking any over-the-counter medications to treat his flu-like symptoms. The patient had equal grips/pushes with a symmetrical smile, no slurred speech, and no arm drift, however the patient's grips/pushes were all weak. The patient has not seen his PCP in over three months, has never been hospitalized, and has not been ill in the past few years.

Physical exam: Unremarkable. ABD soft/supple. No body ulcers noted anywhere on the patient's body.

Vital signs taken approximately 20 minutes after the near syncopal episode while patient was supine:
-The patient appeared to be in mild to no distress.
-A&O x4 with a GCS of 15.
-Skin signs cold, dry, and pale (the patient was from Indian descent and had a naturally dark complexion but was still noticeably pale but not ashen or gray; skin turgor was normal).
-Capillary refill >15 seconds.
-Pupils PERL bilat. 4mm
-Normal Sinus Rhythm at 84 BPM with no ectopy.
-Strong carotid pulse but unable to palpate radial, brachial, or femoral pulses.
-NIBP 40/23 (unsure how accurate that was).
-Respirations 18, non-labored, with adequate tidal volume.
-Lung sounds revealed rhonchi in the upper lobes and were clear in the bases bilaterally.
-SpO2 reading unable to be obtained on his fingers. A disposable adapter was used on his forehead which read 95% on room air.
-Capnography reading was 24 mmHg with normal waveform (no notching, sharkfin, etc.)
-BGL 128 mg/dL.
-12-lead interpretation read, "Normal Sinus Rhythm. T-wave abnormality, consider inferolateral ischemia." No ST-elevation or depression was noted.

Medical history: Hypertension, Migraines.
Surgical history: None.
Medications: Enalapril, Ibuprofen (taken for migraines prn).
Allergies: Bactrim.

Treatment (We do not have dopamine or anything similar in our protocols. Our sole treatment for symptomatic hypotension is NS):

1) Warmed the patient with two blankets and the heater in the back of the ambulance.
2) Established bilateral 14G IV's in the patient's AC region of his arms.
3) Administered a total of 2,000cc warmed NS bolus without change (tubing coiled around a heat pack placed by the heating vent). LS remained unchanged as well. Skin signs remained unchanged.
4) Unable to obtain additional NIBP readings. Radial, brachial, and femoral pulses remained absent. Carotid pulse remained strong.
5) Our STEMI/Stroke Base hospital (20 min ETA) was contacted and given a full patient report. They approved the patient to be transported to the closest paramedic-receiving center (non-specialty) with a 10 min ETA. No orders were given other than to continue with the NS bolus.



Is there anything that any of you would have done differently? What do you think the diagnosis was based on the information provided? I did not get a chance to check up on the patient's status today but I will hopefully in the next week when I work again.
 
First was there any elevation or depression in the Twaves?

He's probably hypovolemic from the N/V/D. As to the cause of that, I couldn't guess. The Rhoncus LS are the only thing stand out to make me question that.

If you can't hang a presser, I can't think of anything to do you haven't mentioned other than place him in Trendelenburg and then transport. Just monitor LS and capnometry due to the fluid bolus.
 
I didn't answer the poll because I don't believe the right answer is there. This guy sounds hypovolemic from gasroenteritis. He may be bordering on SIRS/sepsis but it is not clear cut. Volume replacement and zofran would be the recommended treatment.

Rant#1-trendelenburg does nothing but move organs around
Rant#2-nothing in this scenario is "flu-like symptoms"
[/rant]
 
While reading this, I started thinking along the same lines as ERDoc, the cause possibly being gastroenteritis. As to the "flu-like" statement, I suspect that people think that chills with N/V/D = flu.

Something that I also noticed, how was the BGL measured? If it was by finger stick, it could very well be quite inaccurate. If there's not enough blood flow for the SpO2 sensor to work on the fingers, there might not be sufficient blood flow for the BGL to be measured accurately.

This very well could have been some combination of dehydration from gastroenteritis and some vasovagal reaction because he urinated a very short while before things "went black" on him. I read that combination and thought "micturation syncope" that perhaps didn't quite get to full-on syncope.

Whatever it was, finding out what was might be interesting... or boring. Either way, some of us probably have a little bit of a piqued interest until you can get some follow-up, OP.
 
MS Medic, there was half-a-box elevation in leads I, II, III, and avL in the ST-segment. All of the V leads though were normal. The T-wave itself appeared to be elongated by about twice what it should have been. Sorry I didn't count the boxes for the duration to provide you with better info.

ERDoc, thank you for your input. Is there a way I can edit the post so I can add that option to the poll? Zofran wasn't given because he did not feel nauseated and hadn't thrown up today. I mean't flu-like symptoms as in stomach flu, which is gastroenteritis as you said. I'll change that as well, if I'm able to, in ordr to clarify the scenario a little more clear.

Akulahawk, ya I realize I should have clarified what I mean't as "stomach flu" instead of just saying the flu. After all, the stomach flu isn't really the flu at all, it's gastroenteritis, which has completely different signs/symptoms.
 
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What was his BP after the 2000 of fluids? I'm with the others.
 
Akulahawk - The BGL was taken from the flash of blood in the IV. Some additional info that might add something to the conversation in the meantime, after the third 1,000cc isotonic NS bag drained to approximately 10%, at the hospital, the IV line backfilled quickly with blood. It was at this time that the hospital obtained it's first blood pressure which was 140/53 and a radial pulse could be felt. The pt however, stated that he felt no change and his skin signs remained cold, pale, and dry. This all occurred about 15 minutes after we arrived at the hospital. The only tests that I observed being done were a repeated 12-lead which revealed nothing new, a rectal temp which was 95.3 degrees F, and blood being drawn for the lab. I'll ask some of my co-workers to get an update for me tomorrow, if possible, so I can provide you guys with some more details and hopefully a diagnosis.

Chewy20, after 2,000cc of NS the pt still did not have a radial, brachial, or femoral pulse so we were not able to obtain a BP. He did still have a strong carotid pulse though. Basically from what I observed in the short time I was with the patient, it did not improve his condition at all. The third bag on the other hand, which the hospital hung, may have.
 
Well, now I vote for sepsis.
 
I was thinking sepsis. It all falls inline with severe sepsis. The ETCo2 being around 24, can indicate a lactate being elevated. The low BP and hypothermic core temp are late signs.

Fluids, dopamine, cultures,lactate and abx!
 
ERDoc, I pretty much gave it away by telling you guys the temperature haha; that was my guess from the beginning. Various medics and EMTs that I work with, who saw the pt come in, tried to make a case for hypothermia as to the reason why he was so hypotensive... except hypotension caused by hypothermia is only present with extreme hypothermia and the pt would also first be bradycardic and probably bradypneic which he was not. He also isn't someone you'd suspect to be at risk for hypothermia caused by environmental factors either given his age and the circumstances surrounding the story. My thinking is the rectal temp being <96.8 degrees F and capnography <32 mmHg alone meet generally accepted SIRS criteria. Pair that with the suspected gastroenteritis and the pt now meets Sepsis criteria. Factor in the significant hypotension, which is well <90 mmHg SBP, and he meets Severe Sepsis Criteria. The hypotension didn't improve after mass fluid resuscitation so the pt also meets Septic Shock Criteria-- you could basically check every indicator box on that chart with how he presented. Hopefully I'll have more for you guys soon like the official infection/diagnosis and blood tests (WBC).
 
I think your coworkers are putting things together backwards. Why would someone who is inside a normal house be hypothermic? Hypotension, hypothermia and a source of infection is pretty much the definition of sepsis. I realize that not everyone can get a temp in the field but just the story should lean you that way.
 
ERDoc- I couldn't agree with you more. I'm choosing to believe that they didn't have all of the information before jumping to that conclusion... otherwise God help whoever has that medic/EMT treating them at a critical time. Both our fire departments and ambulance companies don't have thermometers yet, but our county is mandating that they be on every ambulance, ALS or BLS, by the end of 2016 so we will. Heck, we just got capnography nasal cannulas 2 years ago and that has been a game changer for a lot of us. We even had a medic diagnose a pulmonary embolism in the field just last month off the waveform and saved the patient's life because of it.
 
Thanks for the additional info. The low EtCO2 was a bit of a confounder for me at first. Once I saw that low core temperature, and the 2900 mL infusion, I revisited the stuff again and started thinking sepsis too. Regardless of the specific diagnosis, this guy seems to be quite sick.
 
I asked about elevation and depression because you read the machine reading of the monitor which tend to be highly inaccurate. I missed the temperature apparently when reading because I didn't notice the fact that he was hypothermic. With that I'd have gone with sepsis not to be a Johnny come lately.
 
Tell your county to get you lactate monitors as well ;)



But looks like y'all handled the call well. It's weird that y'all don't use pressors, but short of that the PT just needs to be in the hospital getting slammed with fluids and antibiotics.
 
MS Medic, yeah I just listed what the monitor interpreted because I did not disagree with the reading. The monitor's been about 99% accurate for me when I can get the patient to stay completely skill while laying flat, which this guy was perfect for.

Just got a couple updates on the patient for you all. WBC was 53,100/mm3, Neutrophil 47,082/mm3, 34.2% HCT, RBC 3.6 mil/uL, Serum lactate 4.1 mmol/L, PLT 493,000/uL. His blood pressure dropped again almost immediately after I left and they started him on vasopressors and rapid antibiotic therapy. He's been transported to a nearby specialty hospital and is currently intubated and sedated in the ICU. I'm assuming they're also giving him blood transfusions. Either way it is not looking good.
 
Yup drawing a prehospital lactate level could have been helpful with this patient, however if you don't have Dopamine or other vasopressor that would be pretty progressive.

My guess is this guys lactate level would have been through the roof. What you did with the fluid boluses was spot on in my opinion. My guess woulda been hypodynamic (cold) shock/sepsis as well.
 
Yeah the lactate was a dead giveaway, but what's strange is no left shift (the neutrophils were In the normal range), and a left shift normally indicates a bacterial infection.

His hypotension may have been super refractory from the ACE inhibitors he was on; remember the renin-angiotensin axis is the body's primary way to maintain pressure long-term. Sounds like a **** sandwich either way.
 
So, Im going to go out on a limb and be the contrarian on this case. I don't think this was sepsis. I think this was volume depletion from gastroenteritis, but I dont think this gentleman had this syndrome for 3 days and suddenly became septic. He is afebrile, he is mentating, he is not tachycardic and he is not really hypothermic. I think if he was septic with that blood pressure, you would have been dealing with a much sicker patient than you present.

Instead, I would suggest there were possibly two processes going on here. This sounds like run-of-the-mill gastroenteritis to me. But I wonder if this guy had undiagnosed aortic stenosis. First, you say he was of Indian descent. If he had been in the states his whole life, it makes my diagnosis a little less likely. However, outside of first-world countries, rheumatic fever remains prevalent and is the number one cause of aortic valve disease.

Because of the stenotic valve, these patients have fixed cardiac output. They are exquisitely sensitive to volume depletion and when depleted experience hypotension and subsequently syncope. They can increase their peripheral resistance to a point, but without the ability to increase cardiac output, there is a ceiling to their ability to compensate and once that is reached, hypotension ensues.

You mention he had a non-productive cough and you heard noisy breath sounds. I would suggest that what you found was actually the effect of mild pulmonary edema. A heart rate in the high 80's may actually be a relative tachycardia for this man. Because the valve is stenotic, the heart is not able to empty with each systole since the HR has increased (decreased ejection time through a tight valve = incomplete ejection). This causes backup of blood into the pulmonary circulation and leads to the pulmonary edema. And because the heart doesnt have time to empty with each ejection, the cardiac output is actually decreased despite the increase in heart rate. This, combined with the hypotension probably decreased his coronary perfusion pressure and may be the cause of your EKG changes. These patients are exquisitely sensitive to decreases in their coronary perfusion pressures.

Most patients with aortic stenosis have what is called pulsus parvus et tardus. This means that the carotid pulsation is both weaker and slower than it would be in most patients. However, in the face of a blood pressure like this, it may be the only pulse you can palpate because the carotids come off the aortic arch. By the time the slow and weak pulse wave reaches the periphery, it is probably dampened enough to be non-palpable.

If this was the case, you saved this man's life. Fluids are most certainly the answer, despite the possible pulmonary edema. By restoring the patient's volume, you will increase the systemic blood pressure and thus perfuse the coronaries. This will likely slow the heart rate and allow the heart more time to eject blood through that stenotic valve, and likely resolve the pulmonary edema by relieving the backup into the pulmonary circulation.. Vasoconstrictors such as phenylephrine or vasopressin would also be options, though it may seem counterintuitive to raise the afterload on a stenotic valve. But, volume and coronary perfusion pressure are the key factors in treating patients with aortic stenosis. The worst thing you can do to these folks is put them on positive chronotropic drugs. Dopamine may very well have made this patient much worse.

All supposition, but food for thought.
 
I didn't mean to bring this thread to a screeching halt. It was hopping in the wee hours of the morning but suddenly died. I like seeing other people's opinions on these interesting calls. Please don't let my hypothetical diatribe be the last post on this very interesting thread. I keep hitting refresh, and it's making me sad.
 
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