20 yo male with weakness

[pbruss]

One of you may have seen a case similar to this educational case recently at another hospital. If so please do not share the details of your case. The following case is made up but based on a patient I saw recently.


20 yo male comes in with bilat LE weakness and inability to walk over past 10 days. Only pmhx is sickle cell trait. Takes no meds. He is usually healthy, plays football on scholarship at Toledo. Does not drink, smoke or use drugs.

Symptoms started gradually with left upper and pain, ha, neck pain, body aches, fever, cough with blood in his spitum, and tingling in both LE.

He recently saw his PCP and had a few visits to a different ER and an admission to a different hospital. In that time he had multiple tests done including a normal MRI of the brain. A left lower pneumonia was found during this time and he was started on ABX. He also had an LP that showed no meningitis or guillian burre.

He had a bunch of labs done too. The relevant abnormalities were platelet count of 70, mild macrocytic anemia, and a very low reticulocyte count and some Mike rhabdo.

He comes in today because his LE are worse and now is having problems walking without assistance.

His vitals and exam are normal except the LE. He is tender in his left calf but not the right.
Sensation is decreased but intact and the same in both legs. Strength is normal in both UE but 4/5 in both legs. He has positive Babinski's in both feet, almost absent DTRs in both LE. Poprioception is decreased in both LE and normal in UE.

On this visit he has a normal repeat LP, MRI of c spine that is normal, elevated d dimer with DVT of left leg and CTA of chest that shows continued pneumonia but now he has PE.

Shortly before this all started he went to visit family in eastern Virginia for the 4th of July, moved into a new house that had just been extensively renovated, and started conditioning for football which mean they run a lot but no contact and he did not have any injury or trauma.

On this visit his playlets, hemaglibin and retic count are all still low but not worse then the values from his previous workups.

Can anyone come up with a diagnosis? Feel free to ask any further questions or ask for more tests that might help you out.

And again thus is all for educational purposes. Any similarities with actual cases are coincidental.

[kemple]

So I know we discussed this at TTH but there is no more information here than I had there so I"ll take a shot. I'm wondering if there is some weird cord syndrome due to his sickle cell trait cutting off blood supply. This would be a long shot as it's trait not full blown disease, but definitely an interesting case. Not sure you could gat a ct angio of that but would be interesting. Maybe consider treating for sickle cell and see if symptoms start to resolve?

[pbruss]

you are close. him having sickle cell trait did pre-dispose him to acquiring this condition but its not a blood flow problem. the clue of what exactly is causing his problems is in the history he gave but may take some more detailed questioning to figure out what test to order for the diagnosis.

[Bjs04f]

LUQ pain concerns me for splenic infarct, has he had any issues with his spleen in the past? Also that would predispose him to any sort of encapsulated organism or fungus.

[pbruss]

he had an ultrasound of the spleen that was normal at the other hospital. good thought but his issues all start with a non-infectious process.

[Bjs04f]

Has he ever needed any management of his sickle trait, ie. transfusion or use of hydroxyurea

[pbruss]

never.

lets review:
1. he has evidence of soemthing causing problems with the production of blood products.
2. he has something making his blood hypercoagulable.
3. he has something that is affecting his nervous system.
4. he has never had this problem before and the only different things prior to this were moving into a recently renovated house and visiting family in Virginia.

and remember i already gave away that it is not an infectious process

[mcclain]

Lead poisoning from the newly renovated house? Lead paint? Lead does weirdo crap.

[pbruss]

right on. i was concerned about a heavy metal poisoning namely lead and arsenic. however on the trip to Virginia there was a big fish fry of catfish from the local river. found an EPA web sight that recommends zero consumption of catfish from that region due to high mercury levels. this is an example of acute mercury poisoning which i think only he got because of his sickle cell trait which made it easier for him to get symptomatic. see below and attachment.

3.2. Organic Mercury Compounds



Most available data on organic mercury compounds refer to methyl mercury, which is a major source of human mercury exposure, is found naturally in fish, and is relatively stable. Ethyl mercury behaves in a similar fashion to methyl mercury at the cellular level, but with an excretory half life about one third as long [5].



Methyl mercury vapor is absorbed with similar (80%) efficiency as metallic mercury vapor [5]. Intestinal absorption of methyl mercury from fish is also fairly efficient, as is absorption through the skin [5]. On entry to the bloodstream, methyl mercury adheres to sulfhydryl groups, particularly to those in cysteine. Methyl mercury is deposited throughout the body, with equilibrium between blood and body occurring approximately four days after exposure [45]. Distribution to peripheral tissues seems to occur through one or more transporters, especially the cysteine transporter, probably adherent to the sulfhydryl group in cysteine [5].



Concentration of methyl mercury occurs in the brain, liver, kidneys, placenta, and fetus, especially in the fetal brain, as well as in peripheral nerves and bone marrow [5]. Deposited methyl mercury slowly undergoes demethylation to inorganic mercury [46].



The excretory half life of methyl mercury in man is about 70 days, with approximately 90% being excreted in stool. Some degree of enterohepatic circulation apparently occurs. Perhaps 20% of methyl mercury is excreted in breast milk, with the actual amount varying with severity of exposure [5]. Hair mercury reflects blood methyl mercury at the time of incorporation, but not elemental mercury [47], and hence is not a good index of total body burden [5], given the short half life of methyl mercury in blood.



Dimethyl mercury is also efficiently absorbed through the skin, and there is a reported death of a scientist caused by minimal skin contact [48].


Methyl mercury reacts with sulfhydryl groups throughout the body, therefore potentially interfering with the function of any cellular or subcellular structure. Mercury is believed to interfere with DNA transcription and protein synthesis [59], including protein synthesis in the developing brain, with destruction of endoplasmic reticulum and disappearance of ribosomes [60]. Evidence suggests disruption of numerous subcellular elements in the central nervous system and other organs and in mitochondria; adverse effects have also been described on heme synthesis [61], cell membrane integrity in many locations [5], free radical generation [27, 62, 63], neurotransmitter disruption, and stimulation of neural excitoxins [5], resulting in damage to many parts of the brain and peripheral nervous system [5].



Methyl mercury has been associated with reduction in Natural Killer cell activity [64–67], as well as an imbalance in Th2 : Th1 ratios favoring autoimmunity [34, 68, 69]. Mercury is also possibly associated with disruption of DNA repair [5, 27]. The affinity of mercury for sulfhydryl groups of the mitochondrial oxidative phosphorylation complex [70] associated with destruction of mitochondrial membranes may contribute to chronic fatigue syndrome.

Attachments:

Waterbody and Affected Boundaries.docx (14.07 KB)