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Mental Health Follow-up/Progress Note
Patient Name: xxx xxxxxxx Facility: XXXX
Date(s): x-xx-xx Last seen: x-xx-xx
Objective: I was asked to see her again because “she talks to people who are not there… has
bitten a staff member… on occasion has kicked at staff… tried to eat a sock”.
We still don’t have the actual discharge summaries from XXX and XXX. As a consequence,
we don’t know some critical things about her after she was pulled from a burning house: what
were her carboxyhemoglobin levels? How long was she comatose; was she even comatose?
Also we don’t have any of the neuroimaging just second or third hand references to it (11-17-
14 CT Scan of Head 1.) generalized atrophy 2.) nonspecific white matter changes likely
secondary to small vessel disease). We do know that she suffered smoke inhalation on
November 11 which resulted in an anoxic brain injury. Reportedly, she had severe dementia
prior to that.
She currently takes Lexapro 20mg qd, Risperdal 0.5mg bid and 0.5mg q8 hours PRN, Exelon
4.5mg qd
On interview she was extremely distracted humming and singing… experiencing visual
hallucinations (pouring something into her wheelchair) irritable and paranoid; “Who is that?”
Her speech was incoherent and irrelevant. She was restless… grossly confused and disoriented.
Assessment: She remains acutely delirious. The 2/17 labs pointed towards an acute delirium
secondary to compromised renal functioning in a woman with advanced vascular dementia but
the 2/26 lab results nixed that possibility.
There is a rare possibility, delayed postanoxic leukoencephalopathy. Delayed post-hypoxic
leukoencephalopathy (DPHL) is a demyelinating syndrome characterized by acute onset of
neuropsychiatric symptoms weeks or even months following apparent recovery from coma or
delirium after carbon monoxide poisoning. It is diagnosed, after excluding other potential causes
of delirium. The diagnosis can be supported by neuroimaging. The symptoms are those of
encephalopathy (delirium).
Another possibility is a non-metabolically caused delirium such as a new lacunar stroke.
Recommendations/Plan: Would increase her routine Risperdal to 1mg bid. Continue previous
behavioral recommendations and await records from XXX and XXX. The above would require a
brain MRI to rule in or rule out and possibly a neurologist visit. Records later established DPHL
DrewChenelly, Psy.D.
ClinicalNeuropsychologist

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Postanoxic Leukoencephalopathy

  • 1. Mental Health Follow-up/Progress Note Patient Name: xxx xxxxxxx Facility: XXXX Date(s): x-xx-xx Last seen: x-xx-xx Objective: I was asked to see her again because “she talks to people who are not there… has bitten a staff member… on occasion has kicked at staff… tried to eat a sock”. We still don’t have the actual discharge summaries from XXX and XXX. As a consequence, we don’t know some critical things about her after she was pulled from a burning house: what were her carboxyhemoglobin levels? How long was she comatose; was she even comatose? Also we don’t have any of the neuroimaging just second or third hand references to it (11-17- 14 CT Scan of Head 1.) generalized atrophy 2.) nonspecific white matter changes likely secondary to small vessel disease). We do know that she suffered smoke inhalation on November 11 which resulted in an anoxic brain injury. Reportedly, she had severe dementia prior to that. She currently takes Lexapro 20mg qd, Risperdal 0.5mg bid and 0.5mg q8 hours PRN, Exelon 4.5mg qd On interview she was extremely distracted humming and singing… experiencing visual hallucinations (pouring something into her wheelchair) irritable and paranoid; “Who is that?” Her speech was incoherent and irrelevant. She was restless… grossly confused and disoriented. Assessment: She remains acutely delirious. The 2/17 labs pointed towards an acute delirium secondary to compromised renal functioning in a woman with advanced vascular dementia but the 2/26 lab results nixed that possibility. There is a rare possibility, delayed postanoxic leukoencephalopathy. Delayed post-hypoxic leukoencephalopathy (DPHL) is a demyelinating syndrome characterized by acute onset of neuropsychiatric symptoms weeks or even months following apparent recovery from coma or delirium after carbon monoxide poisoning. It is diagnosed, after excluding other potential causes of delirium. The diagnosis can be supported by neuroimaging. The symptoms are those of encephalopathy (delirium). Another possibility is a non-metabolically caused delirium such as a new lacunar stroke. Recommendations/Plan: Would increase her routine Risperdal to 1mg bid. Continue previous behavioral recommendations and await records from XXX and XXX. The above would require a brain MRI to rule in or rule out and possibly a neurologist visit. Records later established DPHL DrewChenelly, Psy.D. ClinicalNeuropsychologist