A little puzzled looking for some input

I had a pt for a few days last week that has just been stuck in my mind and troubling. Last I heard they are looking for an accepting hospital to actually transfer to a higher level of care. However he is self pay so I don't think he will be going anywhere else. I'm not so much looking for a diagnosis, but more so if anyone has seen anything like this before. Pt is a 33 y/o male originally admitted as a non tele pt to med/sug floor for sickle cell crisis. pt had been seen in the ER twice over the past 36 hours before being admitted for the same thing. Treated for pain and sent home. Pt's retic count is finally elevated so pt is admitted and treated with dilaudid IVP not PCA. Less than 24 hours into hospital stay the pt's wife starts reporting AMS and decreased level of consciousness. Doc's still write a d/c order for pt. It is very apparent by midmorning though that the pt is not going anywhere. He stops eating, starts sleeping more, stops talking, and finally just starts staring off and moaning. His eyes start to roll into the back of his head. He had transfer orders to ICU, just waiting on an open bed. About 17:30 I receive him as a transfer into icu. Initial O2 sat of 30's-40's, hr 120's-130's, not following commands, essentially nonresponsive, eyes rolling around and to the back of his head. We got him in Immediatley placed on nonrebreather and discussed a code for intubation and air way protection but his sats rose quickly to the 90's, HR came down with increase in O2 sat. Over the next few days his neuro status has barely improved and he ended up having to move over to bipap but never has required intubation. However if you take the bipap off for more than just a few minutes he has a seizure and desats. He desats as a result of the seizure, not before so I can't seem to tie the two together. I also can't seem to figure out how we went from sickle cell crisis to such a change in mental status. I am curious to see later on if the diagnose him with an anoxic brain injury because his wife said he was having what looked like the seizures he was having in ICU before he came to us but the floor nurse just said it was shivering and put a blanket on him. He has been started on Keppra with no change in the seizures. CT scan was negative for everything. We haven't been able to get an MRI because we don't have a Bipap that can go in there, only a vent is down there and when he comes off bipap he seizes. No other past medical hx except for a cholecystectomy, pneumonia once and a bout of food poisoning. His spleen and liver are now enlarged. Elevated lft's and ammonia increased for 48 but decreased with lactulose. The hematologist said lft's can occur with sickle cell, but it never usually affects the spleen. He is unsure if it was ever sickle cell in the first place. Have you ever seen anything like this before? Sickle cell chest syndrome has been discussed, but it doesn't account for the spleen. Pt also sits at about a temp of 100-101 with Tylenol. Again not looking for a dx, just have you seen anything happen like this before?
Are you sure he said it doesn't affect the spleen? A patient in sickle cell crisis can have damage to the spleen because these "mis-shaped" blood cells can clog the spleen. The blood vessels become blocked and cause damage to other organs. It can affect the lungs, bones, brain, spleen, muscles, eyes and kidneys. Immune system also becomes compromised. The blood cells that are sickled cannot carry oxygen like normal blood cells leading to hypoxia. Hypoxia leading to....and well, you know the rest of the chain of events. He probably has had some strokes as bleeding can occur in the small vessels of the brain that have been damaged by the sickled cells.I don't know...it very well could be soemthing else, but sickle cells crisis is not ONLY pain in joints and such. It can lead to many many other complications.

I was thinking the same thing about the spleen, but it was the hematologist that said it doesn't usually cause enlargement of the spleen. He also did get 2 units PRBC upon arrival to the unit and was getting another one a few days later. I really hope he recovers but his neuro status hadn't improved at all over 4 days.

Hepatic encephalopathy? Fits with the AMS, LFTs, and ammonia.Any history of ETOH abuse or hepatitis? Enlarged liver and spleen due to portal hypertension from cirrhosis?

Just a quick note about his Keppra. When I was weaned off Tegretol and onto Keppra, it took about 10 days to achieve complete seizure control.I did well on the Tegretol but blood values weren't good. The Keppra made me very dizzy and nauseated for the first month and my spleen enlarged slightly despite drug levels being right on target. The solution to the dizziness proved to be taking one and a half tablets instead of two in the morning and the remaining half an hour later and two tablets at bedtime. About two months later, my spleen was back to normal.

I agree with all previous posters, but curious why they didn't start him on dilantin iv for the seizures rather than something that takes longer to be therapeutic? And as for the MRI, hyperoxygenate him with bipap, then do rapid sequence intubation with a paralytic so he doesn't seize, and tube him, then get the MRI. Just my two cents..BeLLaRN

Def sounds like an anoxic event. His blood gasses are ok?

No hx of ETOH or drug abuse. No hx of previous blood transfusions. No hx of hepatitis. I wanted to tube him on arrival to the floor but his O2 status did improve rapidly with the introduction of nonrebreather and then bipap, but also since Diprivan has antiseiuzure effects also. Suprisingly so far his ABG's remained good so we had no other justification for tubing him. I didn't have him the last day I worked but I did notice that his heart rate had decreased from the 70's-80's down to the 40's. I am really curious to know what is going on.

Anybody looking at increased intracranial pressure as a result of cerebral edema post anoxic injury? That'll make you bradycardic.

Quote from GrnTeaAnybody looking at increased intracranial pressure as a result of cerebral edema post anoxic injury? That'll make you bradycardic.

Quote from brilloheadHepatic encephalopathy? Fits with the AMS, LFTs, and ammonia.Any history of ETOH abuse or hepatitis? Enlarged liver and spleen due to portal hypertension from cirrhosis?

I have seen something similar as to what you describe. The pt was in his 40's, AMS, extreme pain, enlarged liver/spleen, fever, increased ammonia levels, almost unresponsive one minute to 4 point restraints etc.. H&H was very low on admission, in the 4 range, only to come up post transfusion then drop even lower. I honestly can't tell you how many units of blood the pt received The pt had Acute lymphocytic leukemia or ALL for short.