78yo Male "Not Acting Right"

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You're ALS ambulance is called to an assisted facility at 0300 for a 78yo male "not acting right." As you arrive, non-medical facility staff inform you that they've received calls from neighbors stating that some sort of commotion is occurring in the patient's room, but that they've never had any issues before.

When you enter the room, you find the patient stumbling about and very confused. Some chairs and wall-hangings have been knocked down. The pt's wife states that the patient went to bed without complaints and was acting normal. She adds that the patient takes "blood pressure pills" but cannot elaborate further on history or medications. The patient has no drug allergies.

You calm the patient enough to get him seated and begin your assessment and find:

Mental Status Exam: Confused, disoriented, restless
Skin: Pale, Cool, Clammy
HEENT: Unremarkable
Lungs: Bilateral rales in bases and halfway up chest
Heart: Obvious rub and gallop noted
Abdomen: Unremarkable
Extremities: No peripheral edema, CMS present/intact x4

Vital Signs: BP: 180/110, HR: 44 irregularly irregular, RR: 30 irregular and noisy, SpO2: 86%, BGL: 126.

What make your list of differentials? What is your primary? How will you treat? What other info do you want, though I'll warn you that you won't get much else.

I have my own ideas about what's going on and will post later. This is scenario that I have worked through as an assignment, but would like further input on considering the vagueness.
 
You're ALS ambulance is called to an assisted facility at 0300 for a 78yo male "not acting right." As you arrive, non-medical facility staff inform you that they've received calls from neighbors stating that some sort of commotion is occurring in the patient's room, but that they've never had any issues before.

When you enter the room, you find the patient stumbling about and very confused. Some chairs and wall-hangings have been knocked down. The pt's wife states that the patient went to bed without complaints and was acting normal. She adds that the patient takes "blood pressure pills" but cannot elaborate further on history or medications. The patient has no drug allergies.

You calm the patient enough to get him seated and begin your assessment and find:

Mental Status Exam: Confused, disoriented, restless
Skin: Pale, Cool, Clammy
HEENT: Unremarkable
Lungs: Bilateral rales in bases and halfway up chest
Heart: Obvious rub and gallop noted
Abdomen: Unremarkable
Extremities: No peripheral edema, CMS present/intact x4

Vital Signs: BP: 180/110, HR: 44 irregularly irregular, RR: 30 irregular and noisy, SpO2: 86%, BGL: 126.

What make your list of differentials? What is your primary? How will you treat? What other info do you want, though I'll warn you that you won't get much else.

I have my own ideas about what's going on and will post later. This is scenario that I have worked through as an assignment, but would like further input on considering the vagueness.

Whoa good case. I'm going to just think outloud [type] here...78 y/o "not acting right I think sepsis, hypoglycemia or stroke as I walk in the door. Sounds like an acute onset, so sepsis is less likely. "blood pressure pills" hmmm, not very helpful, a few classes of drugs there with different toxicity profiles...Physical Exam: skin signs make him look shocky, I'm thinking sepsis again...lungs sounds + heart sounds = CHF with pulmonary edema.

Interesting about "rubs and gallops". Gallops come in 2 flavors, S3 and S4. S4 comes just before systole and indicates aortic stenosis or hypertrophic cariomyopathy. It is the sound of turbulant flow through a narrow space, thats why it is heard just before S1. S3 comes just after systole and indicates an overfilled ventricle (think CHF). S3 is the sound of leftover blood sloshing around in the ventricle after systole, thus it is heard after S2. Given the HPI, I think we are hearing S3. Also, given that he is in AF, he probably doesn't have enough atrial kick to really produce the velocity to create an S3, S4 is more likely given the clinical picture.

It can be difficult, especially in the field, to distinguish S3 and S4, any chance we know which one we are hearing here?

A cardiac friction rub is typically associated with pericarditis. I would expect to see diffuse ST elevation on 12-lead, did we get one? I would also expcect a LOW BP, muffled heart sounds, and JVD (Beck's triad), which we don't see so pericarditis is less likely. Also I would expect some chest pain, and a narrow pule pressure.

Vitals support a CHF exacerbation working Dx. His BP meds might be beta-blocker. If he took too much, his heart rate would slow to something like 44. Alpha adrenergic reponse can raise systemic resistance and we see a rise in BP without a rise in HR (blocked). Heart failure commenses, leading to pulmonary edema, O2 sat drops as his lungs fill with fluid backing up from his heart, he goes loopy from hypoxia and starts stumbling around, confused. His heart is also not happy with its oxygen supply and goes into Afib, further complicating his condition.

Did we get a 12-lead? Jugular venous distention? Do you have CPAP?
 
No EKGs. CPAP available. Nothing else remarkable on physical exam.
 
Temp? Do we know how long he's been off of his meds? Tell us more about how he's acting. What's been going on in the last week?

I am thinking cardiac, and I believe that we could get to the root of the problem with a 12 lead. I do not believe that this is a medication dosage error.

I also want to do a full stroke scale on this guy. Far beyond Cincinnati. His vitals could be a clue to cushing's.

Any recent trauma, btw?
 
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Temp? Do we know how long he's been off of his meds? Tell us more about how he's acting. What's been going on in the last week?

I am thinking cardiac, and I believe that we could get to the root of the problem with a 12 lead. I do not believe that this is a medication dosage error.

I also want to do a full stroke scale on this guy. Far beyond Cincinnati. His vitals could be a clue to cushing's.

Any recent trauma, btw?

I wish I had an EKG, but alas that is not part of the scenario for what ever reason.

No recent trauma, and patient went to bed that even without any sort of oddities. Gross neuro exam shows no deficits, and they won't give me details regarding a cranial nerve exam. Pt is cool and clammy to the touch but no temp is available. :angry:
 
Tough one without a lot more information. What are your thoughts?
 
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Acute Aortic Insufficiency, possibly as a result of Endocarditis or a Dissection.
 
Why is he bradycardic with an irregular pulse?

Beta-blockers blunting sympathetic response, Bradyarrhythmia or more likely PVCs from hypoxia, hypertension, or an intracranial process.
 
I've got lots of thoughts, but my gun to head differential is a CHF exacerbation causing a hypoxic event.

Breakdown of Assessment Findings
MSE: What is causing altered mentation?

•Alcohol: Not likely, potentially contributing
•Epilepsy/Seizure: No history, vital signs and behavior atypical for post-ictal state.
•Insulin: BGL does not point to a blood sugar issue, though patient might be a "functioning hyperglycemic" and this is low for him.
•Overdose: Vital signs do not suggest Beta Blocker overdose or other HTN medication overdose (likely presents hypotensive).
•Underdose: Consider non-compliance with HTN medications causing CVA. Neuro exam likely to be difficult though lack of facial paraesis, extremity CMS deficits and ambulatory patient could constitute a “gross neuro” exam. Pt does fit Cushing’s Triad criteria. Difficult to rationalize a rate of 44 and non-compliance with HTN medications though.
Trauma: Pt appears atraumatic though detained secondary assessment is a must.
•Psych: Does fit well with history considering place of residence and wife.
•Stroke/Shock: See above in regards to stroke. Poor perfusion status secondary to hypoxia needs to be a primary consideration. Skin signs and SpO2 may confirm this, which may cause altered mentation. Could be septic, but daily activities and hypertension seem to contradict this.

Primary Impression: Altered mentation secondary to acute hypoxia/poor perfusion status.

Rule Outs: Acute ETOH intoxication, overdose of other (wife’s) medications, CVA, and trauma. A thorough neuro assessment needs to be done immediately to rule out a CVA, which is obviously a time sensitive issue. Serial stroke scales and a 12 point cranial nerve exam need to be performed.

Why is the patient hypoxic?
Bilateral rales in lungs may indicate inadequate gas exchange is occurring in the lungs because of pulmonary edema. Causes of pulmonary edema include cardiomyopathy, heart valve problems, hypertension, lung infections, kidney disease, adverse drug reactions, and Acute Respiratory Syndrome (ARDS). The patient takes hypertension medications, which may (in addition to the obvious hypertension) indicate valve issues and/or cardiomyopathy. Further questioning of the wife is important to rule out illnesses like recent pneumonia or ARDS. The presence of a gallop (s3) heart tone is often an indicator improperly functioning left ventricle, which is the hallmark of Congestive Heat Failure (CHF).

Congestive Heart Failure is a chronic condition, so what caused this somewhat sudden exacerbation? Pneumonia may cause an acute decompensatation in heart failure patients, or this exacerbation could be the result of uncontrolled hypertension, which may have been caused by patient’s non-compliance with his HTN medications, though the bradycardic rate possibly suggests beta blocker use. The patient has been sleeping in bed supine, which spreads edema through the lungs, worsening the exacerbation. Question wife on recent medication compliance or illness.

What differentiations this patient from CHF and pneumonia?

Working DDx: Pulmonary Edema secondary to a CHF Exacerbation.
long as the airway remains managed, a non-emergent transport is fine.
 
This is a good scenario, for sure.

I like Chase's ddx as well.

The rate and BP mismatch throws me off a bit, and have to wonder if he was quickly trending downward (bradycardic secondary to hypoxia). I'd also not be surprised if he had a heart block.
 
The rate and BP mismatch throws me off a bit

In a normal functioning heart bradycardia can actually cause a degree of hypertension. Slower rate -> Increased filling times -> increased End Diastolic Volume -> Increased force of contraction. Good ol' Starling.
 
In a normal functioning heart bradycardia can actually cause a degree of hypertension. Slower rate -> Increased filling times -> increased End Diastolic Volume -> Increased force of contraction. Good ol' Starling.


:thumbsup:
 
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