Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_208_библиотеки_им_акад_М_И_Перельмана
.pdf
372 Laboratory Medicine in Psychiatry and Behavioral Science
Cushing’s syndrome (CS) (continued)
Nieman LK: Diagnosis of Cushing’s syndrome in the modern era.Endocrinol Metab Clin North Am
47(2):259–273, 2018
Pivonello R, De Martino MC, De Leo M, et al: Cushing’s disease.Endocrine 56(1):10–18, 2017
Ragnarsson O: Cushing’s syndrome—disease monitoring: recurrence, surveillance with biomarkers or
imaging studies. Best Pract Res Clin Endocrinol Metab 34(2):101382, 2020
Santos A, Webb SM, Resmini E: Psychological complications of Cushing’s syndrome.Curr Opin Endocri-
nol Diabetes Obes 28(3):325–329, 2021
Wagner-Bartak NA, Baiomy A, Habra MA, et al: Cushing syndrome: diagnostic workup and imaging fea-
tures, with clinical and pathologic correlation. AJR Am J Roentgenol 209(1):19–32, 2017
https://t.me/med1917
373 Diseases and Conditions
Delirium
Clinical findings According to DSM-5, delirium is characterized by a disturbance in at-
tention and awareness that develops acutely, represents a change from
baseline function, and tends to fluctuate over the course of the day. At
least one other cognitive disturbance must be present in orientation,
memory, language, visuospatial ability, or perception, and there must
be evidence of an underlying condition or conditions to explain the
disturbance. Symptoms often become more florid in the evening or
nighttime hours, and sleep disruption is common and can be so severe
that daytime and nighttime activity patterns are reversed. Changes in
perception can take the form of florid visual hallucinations. Although
not part of the formal criteria, delusions are often present and, coupled
with disorientation, can drive disruptive behaviors such as attempted
elopement. In the case of etiologies such as alcohol withdrawal, auto
-
nomic signs are seen.
DSM-5 categorizes delirium etiologies as substance intoxication, sub-
stance withdrawal, medication-induced, due to another medical con-
dition, or due to multiple etiologies. Underlying diseases commonly
include infection (particularly sepsis, pneumonia, or urinary tract in-
fection), metabolic derangement, electrolyte disturbance, dehydration,
cardiac dysrhythmia, heart failure, stroke, MI, TBI, alcohol/sedative
withdrawal, status epilepticus, and medication toxicity (e.g., with opi
-
oids or anticholinergics). Delirium also commonly occurs following
major surgery, particularly heart surgery.
Delirium is seen in COVID-19 infection, particularly in severe cases
with pulmonary involvement but also in seemingly mild cases without
respiratory symptoms. Both direct brain effects from viral entry and
indirect effects from inflammatory mechanisms have been implicated.
Delirium that emerges during hospitalization for COVID-19 may her
-
ald CNS invasion and a worsening prognosis.
Validated clinical instruments that are useful in diagnosing and mon-
itoring delirium include the following:
• 4AT Rapid Clinical Test for Delirium (www.the4at.com/
4at-download)
• Confusion Assessment Method (americandeliriumsociety.org/
wp-content/uploads/2021/08/CAM-Long_Training-Manual.pdf)
• Intensive Care Delirium Screening Checklist (www.lhsc.on.ca/
media/8367/download)
Laboratory testing Laboratory testing is
performed to determine the cause or causes of
delirium. Basic tests include the following:
•CMP
• CBC with differential and platelets
• Urinalysis (especially in females)
In elderly patients and in non-elderly patients with cardiopulmonary
symptoms, an ECG and chest X-ray are also performed.
https://t.me/med1917
374 Laboratory Medicine in Psychiatry and Behavioral Science
Delirium (continued)
Laboratory testing
(continued)
An EEG may be helpful if the diagnosis of the syndrome of delirium
itself is in doubt, particularly if there is a pre-delirium baseline EEG
study available for comparison. EEGs are very sensitive to delirium if
the test is conducted with proper alerting procedures and is interpreted
by an experienced electroencephalographer. The EEG may also reveal
the presence of non-convulsive status epilepticus, with persistent
symptoms of disturbed attention and awareness.
If the basic workup is unrevealing of a substantial cause of delirium,
the following laboratory studies should be considered:
•ESR or CRP
• Serum ammonia level
•HIV testing
• Antinuclear antibody test
• Vitamin B
12
and folate levels
•RPR
• Urine toxicology
• Blood alcohol level
• Medication levels
• Brain MRI or head CT
• EEG
•CSF analysis
• Blood cultures
• Urine porphyrins
• Arterial blood gases
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Hawkins M, Sockalingam S, Bonato S, et al: A rapid review of the pathoetiology, presentation, and man-
agement of delirium in adults with COVID-19. J Psychosom Res 141:110350, 2020
Hshieh TT, Inouye SK, Oh ES: Delirium in the elderly.Clin Geriatr Med 36(2):183–199, 2020
Jacobson S, Jerrier H: EEG in delirium. Semin Clin Neuropsychiatry 5:86–92, 2000
Klimiec-Moskal E, Slowik A, Dziedzic T: Delirium and subsyndromal delirium are associated with the
long-term risk of death after ischaemic stroke. Aging Clin Exp Res 34(6):1459–1462, 2022
Kotfis K, Williams Roberson S, Wilson J, et al: COVID-19: what do we need to know about ICU delirium
during the SARS-CoV-2 pandemic?Anaesthesiol Intensive Ther 52(2):132–138, 2020
Marcantonio ER: Delirium in hospitalized older adults.N Engl J Med 377(15):1456–1466, 2017
Mattison MLP: Delirium. Ann Intern Med 173(7):ITC49–ITC64, 2020
Thom RP, Levy-Carrick NC, Bui M, Silbersweig D: Delirium.Am J Psychiatry 176(10):785–793, 2019
White L, Jackson T: Delirium and COVID-19: a narrative review of emerging evidence.Anaesthesia
77(Suppl 1):49–58, 2022
https://t.me/med1917
375 Diseases and Conditions
Dementia
Clinical findings Dementia—DSM-5-TR major neurocognitive disorder—is a syndrome
defined by a decline in cognition that is sufficient to interfere with in
-
dependent daily functioning and is caused by a range of neurological,
neuropsychiatric, and medical conditions. The primary dementias
most likely to be encountered clinically include Alzheimer’s disease
(AD), vascular dementia (VaD), dementia with Lewy bodies (DLB),
frontotemporal dementia (FTD), and Creutzfeldt-Jakob disease (CJD).
Importantly, the differential diagnosis of dementia also involves myr-
iad secondary syndromes in which potentially reversible cognitive dys-
function develops because of toxic exposure or vitamin deficiencies, for
example, and these must be excluded in the workup. The syndromic
diagnosis of “dementia” is insufficient for adequate patient care; efforts
must be made to identify the underlying diseases or conditions.
The history of the present illness obtained from the patient and a reli-
able informant arguably contains most of the information needed for
diagnosis. An insidious onset of episodic memory problems with grad
-
ual progression suggests the possibility of AD. A subacute onset and
stepwise progression of deficits suggests cerebrovascular disease. Early
dream enactment behaviors, prominent visual hallucinations, and/or
parkinsonism suggests Lewy body disease. Prominent disinhibition
often mistaken for a primary psychiatric disorder suggests the possi
-
bility of behavioral variant frontotemporal dementia (bvFTD). A very
rapidly progressive course characterizes CJD.
Other critical elements of the history relate to contributing medical con-
ditions such as hypertension, hyperlipidemia, diabetes, history of TBI,
Parkinson’s disease (PD), and stroke. Alcohol and drug use should be
quantified. Use of medications affecting cognition such as hypnotic and
anticholinergic drugs should be specifically queried. Any family his-
tory of dementia, particularly early onset dementia in a first-degree rel-
ative, should be noted. This could suggest the presence of a genetic
form of dementia requiring a separate line of testing.
The mental status examination is a rich source of information about the
patient’s present state, starting with their appearance and general
behavior, which can be disheveled and disinhibited in patients with
bvFTD. Impairments in speech, motor activity, affect, thinking, and
perception all provide evidence in support of disease affecting different
brain regions. Certain patients, including those with AD, may demon
-
strate a remarkable lack of insight, possibly suggesting frontal system
involvement.
The gold standard of cognitive testing involves a neuropsychological
battery directed toward suspected causes of dementia as well as com
-
mon alternatives. Because this level of testing is not universally avail-
able, a clinical screen can be used as an initial proxy measure. At
present, the most commonly used cognitive screening tool is the
Montreal Cognitive Assessment (MoCA; www.parkinsons.va.gov/
resources/MOCA-Test-English.pdf), which takes about 10 minutes and
yields a range of scores from 1 to 30, with a score <24 generally consid-
ered the cutoff for needed follow-up. It should be noted that if a screen
such as the MoCA is used, seemingly trivial individual deficits such as
in cube copying or naming may represent whole domains of impair-
ment that would be found on more detailed testing.
https://t.me/med1917
376 Laboratory Medicine in Psychiatry and Behavioral Science
Dementia (continued)
Clinical findings The physical exam may reveal abnormalities such as focal neurological
(continued) deficits, parkinsonism, evidence of cerebrovascular disease, or evi-
dence of alcohol or drug use that may be contributing to the patient’s
cognitive problems.
Laboratory testing The following tests should be performed for all patients presenting
with cognitive issues:
• CBC with differential
• CMP (includes glucose, electrolytes, LFTs, and kidney function
tests)
•TSH
• Vitamin B
12
and folate levels
• Structural brain imaging: MRI or CT to identify cortical and hippo-
campal atrophy, masses, strokes, white matter disease, NPH, and
other lesions
Depending on the patient’s history and exam findings, the following
tests may be considered:
• Urine toxicology screen
•HIV testing
• FTA-ABS—notRPR or VDRL, both of which are often negative in
patients with dementia due to neurosyphilis
•Chest X-ray
• EEG to identify non-convulsive status epilepticus, periodic com-
plexes of CJD
• CSF for oligoclonal bands, CSF culture for infection, results of
high-volume CSF removal in NPH
• CSF amyloid-β and tau levels in suspected AD
• CSF for real-time quaking-induced conversion (RT-QuIC) analysis
and MRI diffusion-weighted imaging in suspected CJD
• PET scan in suspected AD
• PET or SPECT scan in vascular dementia or FTD
• PET or SPECT scan in suspected DLB or PD dementia
• Iodine MIBG cardiac scintigraphy showing low uptake of MIBG in
suspected DLB or PD dementia
Other tests that may be useful in selected cases:
• Parathyroid function
• Adrenal function
• Heavy metal screening
•ESR or CRP
•Angiogram
• Genetic testing for young patients with first-degree relatives with
early onset dementia (and others)
Note that brain biopsy is indicated only rarely.
Specialized tests for AD are discussed in the Alzheimer’s Disease
entry.
https://t.me/med1917
377 Diseases and Conditions
Dementia (continued)
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Arvanitakis Z, Shah RC, Bennett DA: Diagnosis and management of dementia: review.JAMA 322(16):1589–
1599, 2019
Gale SA, Acar D, Daffner KR: Dementia.Am J Med 131(10):1161–1169, 2018
Gorelick PB, Scuteri A, Black SE, et al: Vascular contributions to cognitive impairment and dementia: a
statement for healthcare professionals from the American Heart Association/American Stroke Asso-
ciation.Stroke 42(9):2672–2713, 2011
Mak E, Su L, Williams GB, O’Brien JT: Neuroimaging correlates of cognitive impairment and dementia
in Parkinson’s disease.Parkinsonism Relat Disord 21(8):862–870, 2015
McKeith IG, Boeve BF, Dickson DW, et al: Diagnosis and management of dementia with Lewy bodies:
fourth consensus report of the DLB Consortium. Neurology 89(1):88–100, 2017
Ricci M, Cimini A, Chiaravalloti A, et al: Positron emission tomography (PET) and neuroimaging in the
personalized approach to neurodegenerative causes of dementia. Int J Mol Sci 21(20):7481, 2020
Younes K, Miller BL: Frontotemporal dementia: neuropathology, genetics, neuroimaging, and treat-
ments. Psychiatr Clin North Am 43(2):331–344, 2020
Yousaf T, Dervenoulas G, Valkimadi PE, Politis M: Neuroimaging in Lewy body dementia.J Neurol
266(1):1–26, 2019
https://t.me/med1917
378 Laboratory Medicine in Psychiatry and Behavioral Science
Dementia with Lewy bodies (DLB)
Clinical findings DLB—one of the most common of the neurodegenerative dementias—
is caused by the aggregation of misfolded α-synuclein protein inside
neurons of the central and peripheral nervous systems. The essential
feature of DLB is dementia, defined as progressive cognitive decline
that interferes with function. Deficits may be particularly prominent
on tests of attention, executive function, and visuospatial ability. Mem
-
ory impairment may not be prominent in early stages but is usually
evident with progression.
Core features of DLB include fluctuating cognition (attention and
alertness), recurrent visual hallucinations that are well formed and
detailed, REM sleep behavior disorder (RBD; which may precede
cognitive decline) and spontaneous parkinsonism. Fluctuation of
symptoms, recurrent visual hallucinations, and RBD typically occur
early and may be persistent.
Supportive clinical features include severe neuroleptic sensitivity, pos-
tural instability, repeated falls, syncope or other episodes of unrespon-
siveness, severe autonomic dysfunction (with constipation, orthostatic
hypotension, and urinary incontinence), hypersomnia, hyposmia, hal-
lucinations in other modalities, systematized delusions, apathy, anxi-
ety, and depression.
In distinguishing DLB from Parkinson’s disease dementia (PDD), a
“1-year rule” applies: If parkinsonism dev el op s m or e t ha n 1 yea r b ef or e
cognitive changes, PDD is diagnosed. If parkinsonism develops con-
currently with cognitive changes (or within 1 year), DLB is diagnosed.
Prodromes to DLB have been identified in which signs and symptoms
indicate that DLB will eventually develop. Although less well studied,
three such prodromal DLB syndromes have been proposed:
• Mild cognitive impairment with Lewy bodies (MCI-LB)
• Delirium-onset prodrome
• Psychiatric-onset prodrome
Because the first symptoms may be seen ≥15 years before dementia
ensues, these prodromes are very likely to come to the attention of psy
-
chiatrists and other behavioral health specialists.
In MCI-LB, objective evidence of cognitive impairment is seen in one
or more domains, most likely in attention-executive and/or visual pro-
cessing. Impairment on tasks of attention, processing speed, and ver-
bal fluency typically constitute the attention-executive deficits, and
impairment on tasks of visual discrimination, assembly, and figure
drawing typically constitute the visual perceptual and spatial deficits.
If memory is affected, deficits in at least one other domain are seen.
Functional status is preserved or minimally affected. Fluctuating cog-
nition is seen, with varying levels of attention and alertness. Recurrent
visual hallucinations may be observed, and RBD may be present. Fea-
tures of spontaneous parkinsonism are seen, including rigidity, brady-
kinesia, and/or resting tremor.
The delirium-onset prodrome of DLB should be suspected when delir-
ium is recurrent or prolonged, in cases where no cause of delirium is
identified, and in patients with progressive cognitive impairment after
delirium resolves. Care should be taken to identify this subpopulation
because antipsychotic and anticholinergic drugs can be harmful for
these patients. Biomarkers noted below may be useful in this context.
https://t.me/med1917
379 Diseases and Conditions
Dementia with Lewy bodies (DLB) (continued)
Clinical findings The psychiatric-onset prodrome of DLB most often takes the form of
(continued) late-onset major depression or psychosis. Psychosis may be florid, with
vivid visual hallucinations and hallucinations in other modalities and
systematized delusions such as Capgras syndrome or phantom boarder
syndrome. Other presentations reported include apathy and anxiety.
Mild cognitive dysfunction can be present but is not predominant and
may fluctuate over time. Complicating surveillance for symptoms of
Lewy body pathology in this context is the fact that psychomotor retar
-
dation resembles the bradykinesia of parkinsonism. Moreover, parkin-
sonism can be induced by antipsychotic medications, and RBD can be
induced by antidepressant medications. Biomarkers noted below may
be useful in the differential diagnosis.
Laboratory testing Biomarkers indicative of DLB include the following:
• Reduced dopamine transporter uptake in basal ganglia on SPECT
or PET imaging
• Abnormally low uptake on
123
iodine-MIBG myocardial scintigraphy
• PSG confirming REM sleep without atonia
Biomarkers that support the diagnosis of DLB include the following:
• Relative preservation of medial temporal lobe structures on CT or
MRI
• Generalized low uptake on SPECT or PET scan with reduced oc-
cipital activity
• FDG-PET showing preserved metabolism of the posterior cingu-
late cortex (the “cingulate island sign”)
• Prominent posterior slow-wave activity on EEG with periodic fluc-
tuations in the pre-alpha/theta range
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Fukatsu T, Kanemoto K: Phantom boarder symptom in elderly Japanese.Psychogeriatrics 22(1):108–112,
2022
Leys F, Wenning GK, Fanciulli A: The role of cardiovascular autonomic failure in the differential diagno-
sis of alpha-synucleinopathies.Neurol Sci 43(1):187–198, 2022
McKeith IG: Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bod-
ies (DL B): repor t of the Conso rtiu m on DLB International Workshop. J Alzheimers Dis 9:417–423, 2006
McKeith IG, Boeve BF, Dickson DW, et al: Diagnosis and management of dementia with Lewy bodies:
fourth consensus report of the DLB Consortium. Neurology 89(1):88–100, 2017
Taylor JP, McKeith IG, Burn DJ, et al: New evidence on the management of Lewy body dementia. Lancet
Neurol 19(2):157–169, 2020
https://t.me/med1917
380 Laboratory Medicine in Psychiatry and Behavioral Science
Depressive disorder due to another medical condition
Clinical findings This diagnosis differs from that of primary depressive disorder in that
it is based on a more limited set of criteria and is characterized by ad
-
ditional signs and symptoms attributable to the medical disorder. The
depression itself involves only a prominent and persistent period of
depressed mood or markedly diminished interest in usual activities.
The presence of a medical condition that could be linked to the depres
-
sion by some physiological mechanism must be established, and this
requires comprehensive evaluation of the patient’s medical history,
family history, current substance abuse and medications, physical and
mental status exams, and laboratory testing. A temporal relationship
between the depressive disorder and the medical condition is helpful,
as is the presence of atypical features of depression.
Medical conditions known to be associated with depressive disorder
include the
following:
• Endocrine diseases—Addison’s disease, Cushing’s syndrome,
hyperparathyroidism, hypothyroidism
• Vitamin deficiencies—Vitamin B
12
, folate
• Neurological diseases—stroke; TBI; epilepsy; multiple sclerosis; or
Alzheimer’s, Parkinson’s, Huntington’s, or Wilson’s disease
• Infections—CJD, HIV, hepatitis C, neurosyphilis, Lyme disease,
West Nile virus
• Malignancies—pancreatic cancer, paraneoplastic syndromes
Laboratory testing Laboratory testing for all patients includes the following:
•CMP
• CBC with differential and platelets
• Vitamin B
12
and folate levels
•TSH
Further testing depends on the results of the
clinical evaluation and the
initial lab results. This may include any of the following (as well as
other disease-specific tests):
•Urinalysis
• Urine toxicology screen
•RPR
•HIV testing
• Blood alcohol level
• Therapeutic medication levels (for TCAs or mood stabilizers)
• Urine pregnancy testing, if indicated
•ECG
• Brain MRI or head CT
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2022
Carroll VK, Rado JT: Is a medical illness causing your patient’s depression? Endocrine, neurologic, infec-
tious, or malignant processes could cause mood symptoms. Curr Psychiatry 8(8):43, 2009
Deng J, Zhou F, Hou W, et al: The prevalence of depression, anxiety, and sleep disturbances in COVID-19
patients: a meta-analysis.Ann NY Acad Sci 1486(1):90–111, 2021
Marsh L: Depression and Parkinson’s disease: current knowledge.Curr Neurol Neurosci Rep 13(12):409, 2013
Robinson RG, Jorge RE. Post-stroke depression: a review. Am J Psychiatry 173(3):221–231, 2016
Seoud T, Syed A, Carleton N, et al: Depression before and after a diagnosis of pancreatic cancer: results
from a national, population-based study.Pancreas 49(8):1117–1122, 2020
https://t.me/med1917
381 Diseases and Conditions
Diabetes insipidus (DI)
Clinical findings DI is a disease characterized by the passage of large volumes of dilute
urine, more than 3 L in 24 hours. The condition is classified into one of
several forms:
• Central or neurogenic DI results from a deficiency of antidiuretic
hormone (ADH), which is produced in the hypothalamus and
stored in the pituitary gland. It arises from injury to the hypothal
-
amus or the pituitary gland. Causes include head injury, stroke,
tumor, surgery, infection, inflammation, aneurysm, and diseases
such as Langerhans cell histiocytosis.
• Nephrogenic DI results from resistance of the kidneys to the actions
of ADH. It arises when the distal renal tubules are unable to reab
-
sorb filtered water. Causes include urinary tract blockage, chronic
kidney disease, hypercalcemia, hypokalemia, and lithium treat-
ment.
• Primary polydipsia results from excessive water intake despite nor-
mal ADH secretion and action. This condition is identified in pa-
tients with major psychiatric disorders and in health enthusiasts.
Excessive drinking can also arise from injury to the hypothalamus
or pituitary gland resulting in a low thirst threshold (dipsogenic DI).
• Gestational DI results from overexpression of an enzyme from the
placenta that metabolizes ADH, causing a deficiency. It is usually
mild and resolves with labor and delivery but can recur with a sub
-
sequent pregnancy.
Signs and symptoms of DI include polyuria (>3 L/day), nocturia, se-
vere thirst, colorless urine, dehydration, weakness, and myalgias. Fa-
tigue, dizziness, confusion, nausea, and, rarely, loss of consciousness
can occur with dehydration. Physical examination may be normal or
may reveal evidence of dehydration, bladder enlargement, or hydro
-
nephrosis (with flank pain or tenderness, pain radiating to the genitals,
and/or bladder enlargement).
Laboratory testing DI is defined as the passage of large volumes (>3 L/24 hours) of dilute
urine (<300 mOsm/kg). Laboratory testing includes the following el-
ements:
• 24-hour urine collection for urine volume determination
• Urine specific gravity
• Simultaneous measurements of plasma and urinary osmolality
• Serum electrolytes and glucose
•Plasma ADH level
• Challenge tests, such as infusion of hypertonic saline stimulating
copeptin (a proxy for ADH), that can distinguish central DI from
primary polydipsia; water deprivation tests to ensure dehydration
and maximal stimulation of ADH are less often used in current
practice.
• MRI of pituitary gland and/or hypothalamus and assay of pitu-
itary hormones other than ADH
• Genetic testing if there is evidence of familial DI
Goo YJ, Song SH, Kwon OI, et al: Venous thromboembolism and severe hypernatremia in a patient with
lithium-induced nephrogenic diabetes insipidus and acute kidney injury. Ann Palliat Med 11(8):2756–
2760, 2021
Refardt J, Winzeler B, Christ-Crain M: Copeptin and its role in the diagnosis of diabetes insipidus and the
syndrome of inappropriate antidiuresis.Clin Endocrinol (Oxf) 91(1):22–32, 2019
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана