Medical scenario

[Sdiver]

Switching gears here.
Here's a good medical call.
The site I got this from has several different diagnosis from its members.
Let's see what the members here come up with.

A 44-year-old woman in moderate respiratory distress for the past two days, she had experienced mild respiratory difficulty, Nausea/vomiting and intermittent vertigo and tinnitus for three days and a headache and back pain for the last week. Her children had complained to her that "she was getting deaf." Low grade temp and has been “In a really bad mood” She appears restless and slightly diaphoretic, Lethargic when not stimulated. Denies Drug or ETOH intake, states she “Can’t remember what meds she has taken today”

PMHX- Bipolar, Sciatica, Fibromyalgia, Migraines, Cardiac w/ 1 stent, HTN

MEDS- Lithium, HCTZ, ASA, Seroquel, Ibuprofen, Gabapentin, OTC Herbals, Indocin

BP- 110/62
HR- 80
RR- 30 labored
SPo2- 90%
Cardiac Monitor- Sinus Rhythm with nonspecific ST-T changes
HEENT- Clear, Headache
Pupils- Clear 3mm
Neck- Clear
Chest- Clr, no pain
Lungs- Diffuse Rales Bilaterally
Abd- Clear
Pel- Clear
Neuro- Clear

What is your Differential DX?
What will your treatment be?
Any Special Concerns or considerations.

[Trapper John]

I am thinking a couple of things are going on here. Most immediate is CHF (diffuse bilateral rales) but also drug interaction/overdose (Seroquel/HTZ/Gabapentin) could give these symptoms. RO hypokalemia. I would admit this patient and get blood chems to RO hypokalemia. Chest films to RO CHF. Control meds to eliminate overdosage and drug-drug interaction.

[Trapper John]

At first take, the 'back of my mind voice' said metabolic alkalosis.

Interested in those blood chems... :munchin

Ooooh, interesting thought ;) What do you think the proximate cause for this would be? Too many Tums :D

I forgot to include to RO pneumonia in the DDx too.

[Sdiver]

And what the hell are those lab monkeys doing?

Remember Doc, this is "Pre-hospital" where we don't have the luxury of labs to treat our patients. We just have the above scenario to work with. ;)

Just wanted to see what different diagnosis we'd come up with over here.
So far so good.
Keep 'em coming folks. :munchin

[doctom54]

Pulmonary embolism is in the DDX

[Trapper John]

Remember Doc, this is "Pre-hospital" where we don't have the luxury of labs to treat our patients. We just have the above scenario to work with. ;)

Ahhh, Man your no fun :p Do we at least get to know the outcome?

[Trapper John]

Pulmonary embolism is in the DDX

Didn't report any thoracic petechiae on physical exam :p

[Sacamuelas]

I am going with a chronic, moderate to severe lithium overdose. Patient is taking numerous medications that cause increased Li concentrations. HCTZ, Ibuprofen, Indocin, gabapentin, and even some OTC herbals all increase serum LI concentrations.

The HCTZ is one of the main culprits seen in interaction overdoses when used by itself. Combining HCTZ with the ingestion of three other KNOWN causes of increased Li levels has to make you consider Li toxicity in your differential diganosis. That is before you even factor in the unknown "herbal" meds that also can increase serum Li levels...


Also, most if not all pertinant findings in history and physical can be onserved in Li toxicity.

:munchin

[Sdiver]

Ahhh, Man your no fun :p Do we at least get to know the outcome?

Yes, I'll post up the outcome later on.

..... and it's YOU'RE ....

Holy crap .... I am no fun, aren't I ????:eek:

[Trapper John]

Yes, I'll post up the outcome later on.

..... and it's YOU'RE ....

Holy crap .... I am no fun, aren't I ????:eek:

:D:D

[Patriot007]

Agree with Lithium toxicity #1. Also have to rule out salicylate toxicity as well.

History and physical sound more tox but need to consider posterior stroke as well as aortic/carotid dissection.

[UWOA (RIP)]

Me ... I was thinking viral infection ....

[Sdiver]

Here's some answers to your questions ..... In BOLD below.

Does she have a stiff neck? ... NEGATIVE

What is her blood glucose level? .... BGL 108

Pedal Edema? ... NONE NOTED

I would look at the heart. ST elevation changes, low O2 sat, dizziness (arrhythmia intermittent) Does she also has some CHF ?(rales) .... SHE DOES HAVE DIFFUSE RALES BILATERALLY ..... REMEMBER, SHE DOES HAVE A CARDIAC HX WITH 1 STENT PLACED

[PedOncoDoc]

Paraciditas? (infected heart sac for the laymen out there reading this)

I believe the term you are looking for is pericarditis.



When I heard this case the first thing that stuck out to me was the tinnitus which is a classic sign of lithium toxicity.

I would be worried about intentional ingestion/overdose in this patient as a cause for her constellation of signs/symptoms and would need to query about suicidality.

[PedOncoDoc]

Yes, my spelling sucks. Thanks.

Come to think of it ASA OD possible?

Would the lithium cause ST changes? If I remember correctly a stint does NOT but I could be wrong. I Google lith OD but did not see tinnitus. I know ASA OD can cause tinnitus as well as SOB. I treated one that had ASA OD but blood levels were high end normal. Turns out that over time ASA can build up at the cellular level but have normal blood levels. The guy was respiratory alkalosis and metabolic acidosis if I remember correctly. This was late 80's early 90's so my memory may be off.

One can OD on almost anything - including water (see polydypsia causing hyponatremia). Aspirin OD is associated with metabolic acidosis and can also cause tinnitus and pulmonary edema (which I believe contributes to the leading cause of death with aspirin poisoning/overdose).

Regarding tinnitus from lithium - this is very well reported - your google-fu must be a bit weak on this one - try searching "lithium toxicity tinnitus" and I'm sure you will get lots of hits from reputable sources that you can select from.

[Sdiver]

Remember, don't kill the messenger.

Here is the Dx ......

Patient was suffering from ASA or Salicylate Toxicity.

Definition of Toxicity

Salicylate toxicity can result from chronic or acute ingestion. Chronic intoxication results from excessive or therapeutic use over a period of 12 hours or longer. Most commonly, this is seen in elderly patients with arthritis or other musculoskeletal problems. Acute intoxication is more likely to be the result of deliberate self-poisoning. Chronic intoxication is seen less frequently and generally has a poorer outcome, because of a low index of suspicion and delay in proper treatment.

In general, the toxic effects of salicylates are seen at serum levels above 30 mg per dL (2.15 mmol per L). Therapeutic levels needed for the anti-inflammatory effects of salicylates range from 15 to 30 mg per dL (1.10 to 2.15 mmol per L). The Food and Drug Administration recommends that the maximum dose of salicylate in a 70-kg person not exceed 3,900 mg in 24 hours for more than ten days.

Pharmacology

Salicylates are weak acids, and thus are rapidly absorbed from the gastrointestinal tract. Peak serum salicylate levels occur within 12 hours of ingestion. Salicylate-induced pylorospasm and the dosage from (effervescent, enteric coated, etc.) can affect the rate of absorption.

Toxic doses of salicylates have a much longer half-life than therapeutic doses. This is due to a shift from first-order to zero-order kinetics as the salicylate metabolic pathways become saturated even at therapeutic levels. When the enzymes are saturated, plasma salicylate concentration rises rapidly, and toxicity occurs.

Clinical Manifestations

Salicylate toxicity should be suspected in any patient with fever, hyperventilation, seizures or coma of uncertain etiology. It is not uncommon for salicylate poisoning to be misdiagnosed initially as diabetic ketoacidosis.

Initial symptoms of salicylate toxicity include tinnitus (followed by hearing loss), vertigo, nausea, vomiting, hyperventilation and agitation. As the serum level rises, metabolic acidosis ensues, resulting in more severe hyperpnea. This is followed by central nervous system deterioration (lethargy, confusion, delirium, convulsions and, eventually, coma). Fever, due to uncoupling of oxidative phosphorylation, is also a common symptom.

Other manifestations of salicylate toxicity include non-cardiogenic pulmonary edema, renal tubular damage, bleeding disorders and hemolysis. The pathophysiology of salicylate damage to the lungs and kidneys is still unclear, but a central factor seems to be a disruption of capillary permeability to protein, producing high concentrations of protein in both pulmonary edema fluid and urine. A similar phenomenon occurs in cerebral membranes and may produce cerebral edema.

INITIAL TREATMENT

As with any acutely ill patient, initial treatment should focus on establishing an adequate airway, breathing and circulation. The history should include the amount of salicylates ingested, the type of preparation and the exact time of ingestion.

Important initial laboratory tests include an arterial blood gas determination and serum salicylate level, as well as serum sodium, potassium, urea nitrogen and glucose levels and coagulation profile. There are rapid screening tests, such as the ferric chloride test, to detect the presence of salicylic acid in the urine.

IPECAC AND GASTRIC LAVAGE

Gastric emptying should be performed as early as possible by either induced emesis should attemtp to prevent drug absorption by gastric emptying and the use of activated charcoal.

Central to the management of these patients is the use of intravenous fluids and bicarbonate to produce alkaline diuresis and to correct acid-base and electrolyte abnormalities. These patients should be monitored closely and treated aggressively; in some patients, hemodialysis may be necessary.


* Unknown what her labs were.
* Unknown if this was a suicide attempt.

[Sacamuelas]

Classic presentation of a drug overdose/interaction case. :cool:

[Trapper John]

:lifter That was fun. Let's do it again. :D

[Sdiver]

See, Trapper, metabolic alkalosis wasn't TOO far off. :D:rolleyes:

When you posted your Dx right away as alkalosis, I was thinking, "Oh wow, this Doc is good." But then you second guessed yourself and then I was like, "YES, we've got something here." :D

I agree- one more, please.

How about letting us ask the Pt a few questions next time, Sdiver? Just pretend you're a 44 y.o. woman in pain.

Sure. Be more than happy to.
In fact, let me see if I can embed a video for everyone.

[UWOA (RIP)]

Whoopie!

[Patriot007]

Great case and good overview Sdiver!

To clarify treatment as far as recent literature is concerned:

Controversial but generally, induced vomiting is no longer recommended due to the risk of aspiration.

Gastric lavage and aspiration ("stomach pumping") is only recommended if the ingestion has been within 1 hour of ingestion. Typically use a 28 French Ewald tube(Big honkin' tube!) that can only go down if patient is intubated- aspirate flush with saline then aspirate for pill fragments if you get pill fragments rinse and repeat.

Charcoal is nasty thick stuff and due to risk of dangerous aspiration is only recommended if patient has normal neurologic function or is intubated.

In the field it is important to gather evidence of co-ingestions,OTC or prescription bottles, and as much bystander info as possible so that doses can be estimated.

Lastly- aspirin in one of the drugs that can be dialyzed so mistriage to a small department where dialysis will not be possible may cost valuable time. If you have good evidence of a particular overdose discuss with medical control early. They may also give you a contingency treatment plan if the patient decompensates en route in addition to standard ACLS.