dr prashant shringi DM neurology resident

1. Clinical Approach to
Acute Confusional State
Dr Prashant Shringi
Senior Resident

2. Introduction
• Altered mental status can be divided into 2
major subgroups:
• Acute (delirium or acute confusional state)
• chronic (dementia).

3. • A third entity, encephalopathy
• (subacute organic brain syndrome),
denotes a gray zone between delirium and
dementia; its early course may fluctuate,
but it is often persistent and progressive

4. Definition
• Delirium is an acute mental status
change characterized by abnormal and
fluctuating attention.
• Disturbance in level of awareness and
reduced ability to direct, focus, sustain,
and shift attention
• Bradelys Neurology 7 edition

5. synonyms
• Delirium,
• Altered mental status,
• Acute organic syndrome,
• Acute brain failure,
• Acute brain syndrome,
• Acute cerebral insufficiency,
• Exogenous psychosis,
• Metabolic encephalopathy,

6. Subtypes of delirium
• Subtypes: three subtypes-•
 Hyperactive delirium
 Hypoactive delirium
 Mixed type.

7. Subtypes of delirium
• Hyperactive delirium is characterised by agitation,
restlessness and attempts to remove invasive
tools.(Drug Intoxication)
• Hypoactive delirium is characterised by
withdrawal, flat affect, apathy, lethargy and
decreased responsiveness.
• Mixed delirium occurs when the patient’s
symptoms fluctuate between the two conditions .

8. Subsyndromic delirium (SSD)
Patients show one or more symptoms of
delirium (disattention, disorganised
thinking, hallucinations and delusions), but
do not progress to the point that it is
possible to diagnose delirium.

9. Dementia-superimposed delirium
• DSD, An acute change in mental state
(characterised by fluctuating course,
inability to maintain attention,
disorganised thinking or altered state of
consciousness) occurring in a patient
already suffering from dementia

10. Sundowning syndrome
• Sudden changes in behaviour or mental
state
• May be considered circadian variations of
symptoms
• Mid phase of Alzheimers disease

11. DSM-5 Diagnostic Criteria

12. Pathophysiology
• Delirium is the final common pathway of
many pathophysiological disturbances
that reduce or alter cerebral oxidative
metabolism

13. Pathophysiology
• Alteration in cortical brain function, with
abnormalities of deep brain structures.
• These conditions result from
• (1) an exogenous insult or an intrinsic process
that affects cerebral neurochemical functioning
• (2) physical or structural damage to the cortex,
subcortex, or to deeper structures involved with
memory.

14. Pathophysiology
• End result of these disruptions of function
or structure is impairment of cognition
that affects some or all of the following:
• Alertness, orientation, emotion, behavior,
memory, perception, language, praxis,
problem solving, judgment, and
psychomotor activity.

15. How Common ?
• Delirium is by far the most common
behavioral disorder in a medical-surgical
setting.
• In general hospitals -
• prevalence -ranges from 15% to 24% on
admission.

16. • Incidence -ranges between 6% and 56% of
hospitalized patients,
• 11% to 51% postoperatively in elderly
patients,
• 80% or more of intensive care unit (ICU)
patients
• delirium as ‘prevalent’ when it is detected at
admission, and ‘incidental’ when it develops
during the hospital stay

17. Multi-factorial aetiology

18. Major Causes Of delirium
• Metabolic
• Toxic
• Infectious
• Neurologic
• Perioperative

19. Causes

20. Differential diagnosis of acute
confusional state / delirium
• Neurological causes:
• stroke
• traumatic brain injury, subdural haematoma
• infectious encephalitis/meningoencephalitis
CNS vasculitis, limbic encephalitis ,
granulomatous meningoencephalitis (TB,
sarcoidosis)
• non-convulsive status epilepticus
• migraine

22. • Non-neurological causes:
• hypoxia
• hypoglycaemia,
• hyperglycaemia
• hyponatraemia (“dilution delirium”)
• hypernatraemia
• hypocalcaemia, hypercalcaemia

23. • Hepatic encephalopathy
• Adrenal/pituitary insfficiency
Uremic encephalopathy
• vitamin B1 deficiency (Wernicke’s
encephalopathy)
• hyper viscosity syndrome
• acute porphyria

24. • Drugs:
• Levodopa
• Dopamine agonists
• Anticholinergics
• Antidepressants
• chemotherapeutics
• Intrathecal medications
• Steroids

25. • Miscellanious:
• Malignant neuroleptic syndrome
• Serotonin syndrome
• Alcohol withdrawal (“delirium tremens”)
• Benzodiazepine/barbiturates withdrawal

26. Multifactorial origin:
• intensive care (“ICU delirium”)
• postoperative
• advanced cancer
• older patients

28. Diagnostic Difficulty
Delirium
Dementia Psychosis

30. Diagnostic work-up of patients with
delirium
• History
1 vulnerability profile•
2 triggering factors•
3 known medical, neurological,
psychiatric disorders

31. • clinical examination•
• 1 mental status
2 focal neurological signs•
3 other neurological symptoms/signs
•
• 4 other medical findings

32. Investigations•
• Laboratory Profile•
• Neuroimaging
• Cerebrospinal fluid•
• EEG
• Toxicological screening
• ABG

33. History
• Attempt to obtain a current and past
history from other sources, including
prehospital workers, family or friends, and
past medical records
• Look specifically for street drug, alcohol,
and medication use

34. History
• Preexisting endocrine disorders
• Recent activities that may have resulted in
exposure to toxins or environmental injury.
• Psychiatric illness and similar episodes of
confusion in the past, to uncover a treatable
or modifiable cause for the cognitive
impairment.

35. Physical Examination
• Delirious patient should be evaluated for
pupillary, fundoscopic, and extraocular
abnormalities, nuchal rigidity, thyroid
enlargement, and heart murmurs or
rhythm disturbances

36. Physical Examination
• Pulmonary examination that reveals
wheezing, rales, or absent breath sounds
• Abdominal examination that reveals
hepatic or splenic enlargement
• Cutaneous examination that shows rashes,
icterus, petechiae, ecchymoses, track
marks, or cellulitis.

37. Simplified diagnostic criteria: Confusion Assessment
Method (CAM)
Criteria Present?
1. Acute onset and fluctuating course
(Is there an acute change in mental state? Did this
fluctuate during the past day?)
Y / N
2. Inattention
(Is the patient easily distracted or does he have difficulty
keeping track of what is being said?)
Inattention can also be detected by asking for the days of
the week to be recited backwards
Y / N
3. Disorganised thinking
(Is the patient’s speech disorganised, incoherent, rambling,
irrelevant, unclear/illogical or unpredictable switching
between subjects?)
Y / N
4. Altered level of consciousness
(Is the patient vigilant (hyper-alert) or lethargic/drowsy?)
Y / N
1 + 2 + either 3 or 4 must be present to diagnose delirium.

39. EEG and DELIRIUM
• Delirious patients showed significant
reductions of alpha percentage, increased
theta and delta activity and slowing of the
peak and mean frequencies

40. • Engel and Romano (1959) described
alpha slowing with delta and theta
intrusions on electroencephalograms
(EEGs) and correlated these changes with
clinical severity.
• Treating the medical cause resulted in
reversal of EEG changes of delirium.

42. Management
• Non-pharmacological prevention:
• English National Clinical Guideline Centre has
issued guidelines for nonpharmacological
intervention -
• Organisational interventions
• Orientation interventions
• Relaxation interventions

43. • Clinical management interventions
• Promptly correcttion of hypoxia,
hypo/hypertension
• Anaemia and cardiac arrhythmias.
• Ensure adequate enteral hydration

44. • Ensure intake of an adequate amount of
calories, trace elements and vitamins,
preferably through the enteral route
• Suspend unnecessary drug treatments,
especially neuroactive drugs

45. Pharmacotherapy
• Haloperidol – max dose upto 5 mg
• Atypical antipsychotics— risperidone,
olanzapine, quetiapine, and aripiprazole
• Valproate ,ondansateron, Melatonin

46. • Recent evidence indicates that low dose
melatonin and Ramelteon, a melatonin
receptor agonist, are effective at lowering
the risk of delirium .
• NEWER DRUG: Dexmedetomidine, ( alpha-
2 agonist)

47. Management

48. Conclusion
• First, search for delirium! Get used to
the different monitoring tools
• Preventing is better than curing:
prevention is the most effective way to
reduce delirium incidence.
• Search early for risk factors

49. • Always try to use the lowest effective
doses of neuroactive drugs, especially
sedatives: less is better!
• Treat delirium as a medical emergency
aggressively search for underlying
organic/metabolic causes, use of
deliriogenic drugs

50. •
• Thank You

51. Refrences:
• Bradleys' Neurology 7 edtion
• G. Mistraletti et al. / Best Practice & Research Clinical
Anaesthesiology 26 (2012) 311–326Bassetti CL.
• Differential diagnosis and management of non-psychiatric acute
confusional states. Schweiz Arch Neurol Psychiatr. 2007;158:368–78.
• EEG spectral analysis in delirium KOPONEN et al ; Journal of
Neurology, Neurosurgery, and Psychiatry 1989;52:980-98
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