hermanding
JUB Addict
- Joined
- Dec 8, 2006
- Posts
- 4,303
- Reaction score
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- Location
- Los Ange;es
- Website
- justusboys.com
First, about four months before leaving Bogotá, Lalo began incontinence at night. It was not apparent in day. After he got to the States, over time 3 months or so, it was worse, and I noticed that when I came up from Bogotá to see him. He also had a right hydrocele - and guys, this thing was the size of a small tennis ball - just gigantic. You could put 10 of my pelotas inside the volume of it.
Anyway, I am going to quote from his medical records on various days, before asking a question. Remember that he went to emergenci on 24 august with 186-129 pressure and never walked again, although he walked into the er room unassisted.
26 aug - a US renal bilat complete
the bilat hydronephrosis persisted even after foley catheter insertion, which demonstrated a markedly thickened bladder, likely due to muscular wall hypertrophy secondary to cronic outlet obstruction due to enlarged prostate. still incomplete drainage of bladder, even following foley catheter isertion. urinary bladder is markedy distended, even though patient indicated he voided prior to arriving in ultrasound. bladder volume is judged to be 1000 cc.
ct scan of abdomen and pelvis revealed bilat hydroneprosis with dilated ureters down to bladder.
27 aug - from a cardiac dignostic report
patient heart failure status assessed as NYHA class II, with CHF symptoms of DOE
28 aug - from a comprehensive metabolic panel
CREAT 1.7H BUN 15 Potassium 4.0 and others
30 aug - after CABG, pulmonologist consult for respiratory failure (impressions)
coronary artery disease, status post coronary artery bypass grafting.
substantial blood loss anemia with multiple transfuions
shocks likely hemorrhagic, but cardiac tamponade is not excluded
renal disease and other problems
02 sep - bilat renal ultrasound
severe bilat hydronephrosis again seen
foley catheter noted withn bladder
appears to be 7 cm. echogenic focus within bladder. may represent blood or mass or clot
prostate gland is enlarged
10 sep - MRI of brain WO contrasts
multiple focal lacunar infarcts in basal ganglia bilaterally & in parasagittal frontoparietal regions bilaterally & in temporal lobes bilaterally
on previous CT presumed to be old infarcts but in fact are acute infarcts & have occurred in the watershed distribution
///question here - can someone talk a little about 'lacunar' and 'watershed distr'? please. could this be an area where infarcts could cause destruction of bowel control?
18 sep - from basal metabolic panel
BUN 33H creatinine 1.8H among others
23 sep - from an MRI brain wo contrast
multiple focal areas of restricted effusion are aqain noted scattered in periventirulcar white matter. consistent with multiple small lacunar infarcts in watershed distribution. minimal changes of microangiopathy identified.
/// question - again, does any of this help to confirm bowel control loss?
02 oct - report from a chest XR
advanced heart failure pattern
14 oct - from a basic metabolic panel
creat 2.5H BUN 74H potassium 4.5 among others
//he failed a swallowing test by speech pathologist, although later he became able to swallow and not aspirate more than not.
21 oct - from a cystoscopy by urologist - perhaps to me most fascinating of all
procedures - cystoscopy/bilat retrograde pyleogrm/inertion of bilat ureteral stents/evacuation of bladder clot
in the operative notes during the cystoscopy -
prostate was not particular obstructed. bladder mucosa examined. some inflammation, but also a large amount of ORGANIZED clot, which had obviously been there for a considerable length of time. this could not be easily flushed out. an ellik evacuator was used to flush out a part of clot. since the clot was so solid that a resectoscope needed to be used in order to break the clot down into smaller pieces for flushing out. there was moderate trabeculation......ureter was so dilated i was never able to get enough dye into upper collecting ystem. i suspect ureters are obstructed at the UVJ from cronic bladder outlet obstruction.......i started continuous bladder irrigation since patient's INR was significantly elevated. h opefully, we can stop the CBI tomorrow.
///question - organized? for a clot. trabeculation? and such a solid clot. the urologist says - considerable length of time. could this possibly have been going on for say 5 years, 1 year, 2 months - any reasonable ideas on this?
29 oct - from a basic metabolic panel
creat 1.7H BUN 25H potassium 4.6 among others
well, enough records.
it is obvious that Lalo had really bad issues that one would not think arrived at the point of what was seen in the hospital all that quickly. whether he was asymptomatic of everything or not, no one will ever know still on earth.
Although he died 168 days after walking into the emerg room, i am inclined to feel he would have died before that if he had not gone. Many nights as I lay in the bed, I feared i would wke up to find Lalo dead. He was very tired all the time.
If he had symptoms etc - outside of the obvious hydrocele - then he contributed to his own death. If he did not, then he went to emergency under my prodding, and SEEMED to be worse than before - certainly from the point of the probabilities that strokes destroyed smooth muscle functions that are so heavily taught in our society. Before 24 august, I feared he was a death waiting to happen, so different from what I had known.
I APPRECIATE so much any medical experience and lay experience that you might offer. I am at peace with his going, maybe mostly because I saw it coming for much of those 168 days. Accepting his death of course is a process. I am trying to offer you guys clues to maybe answer the medical reasons for his death. Why in the grand scheme does not interest me at all. We all die, some less painfully that others. I am so glad I was with him when he gave it up. He was destroyed, except in his mental capacity - and, even that may have been importuned last Saturday, because the last day he never gave me anything to indicate he was responsive.
my gratitude to all of you
ding
Anyway, I am going to quote from his medical records on various days, before asking a question. Remember that he went to emergenci on 24 august with 186-129 pressure and never walked again, although he walked into the er room unassisted.
26 aug - a US renal bilat complete
the bilat hydronephrosis persisted even after foley catheter insertion, which demonstrated a markedly thickened bladder, likely due to muscular wall hypertrophy secondary to cronic outlet obstruction due to enlarged prostate. still incomplete drainage of bladder, even following foley catheter isertion. urinary bladder is markedy distended, even though patient indicated he voided prior to arriving in ultrasound. bladder volume is judged to be 1000 cc.
ct scan of abdomen and pelvis revealed bilat hydroneprosis with dilated ureters down to bladder.
27 aug - from a cardiac dignostic report
patient heart failure status assessed as NYHA class II, with CHF symptoms of DOE
28 aug - from a comprehensive metabolic panel
CREAT 1.7H BUN 15 Potassium 4.0 and others
30 aug - after CABG, pulmonologist consult for respiratory failure (impressions)
coronary artery disease, status post coronary artery bypass grafting.
substantial blood loss anemia with multiple transfuions
shocks likely hemorrhagic, but cardiac tamponade is not excluded
renal disease and other problems
02 sep - bilat renal ultrasound
severe bilat hydronephrosis again seen
foley catheter noted withn bladder
appears to be 7 cm. echogenic focus within bladder. may represent blood or mass or clot
prostate gland is enlarged
10 sep - MRI of brain WO contrasts
multiple focal lacunar infarcts in basal ganglia bilaterally & in parasagittal frontoparietal regions bilaterally & in temporal lobes bilaterally
on previous CT presumed to be old infarcts but in fact are acute infarcts & have occurred in the watershed distribution
///question here - can someone talk a little about 'lacunar' and 'watershed distr'? please. could this be an area where infarcts could cause destruction of bowel control?
18 sep - from basal metabolic panel
BUN 33H creatinine 1.8H among others
23 sep - from an MRI brain wo contrast
multiple focal areas of restricted effusion are aqain noted scattered in periventirulcar white matter. consistent with multiple small lacunar infarcts in watershed distribution. minimal changes of microangiopathy identified.
/// question - again, does any of this help to confirm bowel control loss?
02 oct - report from a chest XR
advanced heart failure pattern
14 oct - from a basic metabolic panel
creat 2.5H BUN 74H potassium 4.5 among others
//he failed a swallowing test by speech pathologist, although later he became able to swallow and not aspirate more than not.
21 oct - from a cystoscopy by urologist - perhaps to me most fascinating of all
procedures - cystoscopy/bilat retrograde pyleogrm/inertion of bilat ureteral stents/evacuation of bladder clot
in the operative notes during the cystoscopy -
prostate was not particular obstructed. bladder mucosa examined. some inflammation, but also a large amount of ORGANIZED clot, which had obviously been there for a considerable length of time. this could not be easily flushed out. an ellik evacuator was used to flush out a part of clot. since the clot was so solid that a resectoscope needed to be used in order to break the clot down into smaller pieces for flushing out. there was moderate trabeculation......ureter was so dilated i was never able to get enough dye into upper collecting ystem. i suspect ureters are obstructed at the UVJ from cronic bladder outlet obstruction.......i started continuous bladder irrigation since patient's INR was significantly elevated. h opefully, we can stop the CBI tomorrow.
///question - organized? for a clot. trabeculation? and such a solid clot. the urologist says - considerable length of time. could this possibly have been going on for say 5 years, 1 year, 2 months - any reasonable ideas on this?
29 oct - from a basic metabolic panel
creat 1.7H BUN 25H potassium 4.6 among others
well, enough records.
it is obvious that Lalo had really bad issues that one would not think arrived at the point of what was seen in the hospital all that quickly. whether he was asymptomatic of everything or not, no one will ever know still on earth.
Although he died 168 days after walking into the emerg room, i am inclined to feel he would have died before that if he had not gone. Many nights as I lay in the bed, I feared i would wke up to find Lalo dead. He was very tired all the time.
If he had symptoms etc - outside of the obvious hydrocele - then he contributed to his own death. If he did not, then he went to emergency under my prodding, and SEEMED to be worse than before - certainly from the point of the probabilities that strokes destroyed smooth muscle functions that are so heavily taught in our society. Before 24 august, I feared he was a death waiting to happen, so different from what I had known.
I APPRECIATE so much any medical experience and lay experience that you might offer. I am at peace with his going, maybe mostly because I saw it coming for much of those 168 days. Accepting his death of course is a process. I am trying to offer you guys clues to maybe answer the medical reasons for his death. Why in the grand scheme does not interest me at all. We all die, some less painfully that others. I am so glad I was with him when he gave it up. He was destroyed, except in his mental capacity - and, even that may have been importuned last Saturday, because the last day he never gave me anything to indicate he was responsive.
my gratitude to all of you
ding









