Report on Aetiology of Acute Confusional State

Report on Aetiology of Acute Confusional State


Confusional states and coma are among the most common problems in general medicine. They account for a substantial proportion of admissions to emergency wards and are a frequent cause of distress on all hospital services.1

Acute confusional state is a neuropsychiatric syndrome which is difficult to exactly define but involves abnormalities of thought, perception and levels of awareness. It occurs acutely or subacutely and symptoms fluctuate. It is very common, especially in the elderly and many of these patients subsequently do not return to their baseline function and some even require institutionalization.

Confusion and delirium always signify a disorder of the nervous system. They may be the major manifestation of a head injury; a seizure; drug toxicity (or drug withdrawal); a metabolic disorder resulting from hepatic, renal, pulmonary or cardiac failure; a systemic infection; meningitis or encephalitis; or a chronic dementing disease.1

As the etiology of acute confusional state are numerous and presentation also variable, so many time create confusion regarding the actual diagnosis and thus delay the prompt management which may result in fatal outcome. Acute confusional state is thus associated with high rate of mortality and morbidity, specially if undiagnosed. Inouye estimated in-hospital mortality of more than 20%, and mortality within a year of 35-40%.2 Ely and colleagues also found that delirium was an independent predictor of both mortality and longer hospital stays.3 The morbidity and mortality rates depend heavily on the patient’s reason for admission and associated medical illnesses.

Proper and prompt management could only be possible if the etiology of acute confusional state could be diagnosed accurately and thus fatal outcome could be prevented. Therefore an awareness regarding the common causes of acute confusional state is essential for all level of medical practitioner for its early diagnosis, proper treatment and prevention as well.

A lot of studies on acute confusional state have been carried out in many parts of the world in Bangladesh many causes of acute confusional state are being detected but no such acceptable data found.

The present study is based on hospital admitted patients in medicine wards of DMCH during that period of July’ 08 to October’ 08. This study may to some extent reflect the common state prevailing in our country.


Before going into detail of Acute Confusional State the definition of consciousness and confusion need to be clarified.
Means a state of wakefulness with awareness of self and surroundings. 4
Means altered consciousness – the subject is bewildered and misinterprets his/her surroundings.4
Confusion is a mental and behavioral state of reduced comprehension, coherence and capacity to reason.1
Acute Confusional State
Synonyms: Acute brain failure, acute organic reaction, delirium.
Definition: Acute Confusional State is defined as a transient disorder of cognition and attention accompanied by disturbances of the sleep-wake cycle and psychomotor behavior.5 The key feature of delirium is the inability to maintain a coherent stream of thought or action, along with an impairment in attention and/or arousal. Patients cannot keep attention focused, and this attentional disorder underlies many of the other cognitive deficits. Delirious patients are distractible, may be hypersensitive to stimuli, and cannot prioritize important from irrelevant environmental sounds or sights.

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR)6 defines delirium as the following:
• Disturbance of consciousness (ie, reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention

• A change in cognition (such as memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance that is not better accounted for by a preexisting, established, or evolving dementia

• The disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day.

• Evidence from the history, physical examination, or laboratory findings shows that the disturbance is caused by the direct physiological consequences of a general medical condition.

There are 7 signs of acute confusional state-
1. Consciousness is impaired with onset over hours or days. Impaired consciousness is difficult to describe. This has been described more formally as a mild impairment of thinking, attending, perceiving and remembering – or more simply as a mild global impairment of cognitive processes associated with a reduced awareness of the environment. Conscious level fluctuates throughout the day with confusion typically worsening in the late afternoon and at night.

2. Disorientation in time and place is the rule.

3. Behaviour: inactivity, quietness, reduced speech and perseveration or else hyperactivity, noisiness and irritability.

4. Thinking: slow and muddled, commonly with ideas of reference or delusions.

5. Perception: disturbed, often with illusions and visual hallucinations or tactile.

6. Mood: lability, anxiety, perplexion, fear, agitation or depression.

7. Memory: impaired. Later patients may be amnestic for this episode.


Consciousness is a state expressed in two dimension: wakefulness and self aware congnition of past events and future anticipations which accompany the normal wakeful state.

Wakefulness or alertness is maintained by a diffuse system of upper brainstem and thalamic neurons, the reticular activating system (RAS) and its connections to the cerebral hemisphere as a whole. Therefore depression of either hemispheral or RAS activity may cause reduced wakefulness.

Awareness is dependent on integrated and organized material thoughts, subjective experience, emotion and mental process, each of which resides to some extent in anatomically defined regions of the brain.

Altered consciousness is produced by three mechanisms4 affecting –
• Brainstem
• Cerebral cortex

1. Diffuse Brain Dysfunction –
Generalized severe metabolic or toxic disorders (eg alcohol abuse, sedative drugs, uremia and septicemia) depress or inhibit overall brain function.

2. Direct Effect Within the Brainstem –
A lesion within the brainstem itself damages or inhibits the RAS.

3. Pressure Effect on the Brainstem
A mass lesion within the brain compresses the brainstem, inhibiting the ascending RAS.

• Hypoactive subtype –
Apathy and quiet confusion are present and easily missed. This type can be confused with depression.

• Hyperactive subtype –
Agitation, delusions and disorientation are prominent and it can be confused with schizophrenia.

• Mixed subtype –
Patients vary from hypoactive to hyperactive.


Acute Confusional State occurs in about 15 to 20% of all general admissions to hospital.9 The incidence is higher in elderly people and those with preexisting cognitive impairment.

• Virtually all studies of delirium have found age to be a predictor of acute confusional states. Aging changes in the brain, and especially preexisting cognitive deficits or strokes, render the nervous system more sensitive to toxic or metabolic insults, such as medication side effects, electrolyte imbalances, endocrine disorders and renal or hepatic failure, and infections, among many other conditions.
• Elderly patients may have exaggerated responses to over-the-counter and prescription medications with anticholinergic activity.
• Acute encephalopathies develop in 30 to 50% of hospitalized patients older than age 70.10
• A review by Brown and Boyle in the British Medical Journal estimated that a fourth of hospitalized patients older than age 65 develop delirium during hospitalization.10

A recent study of delirium in older patients admitted to a general internal medicine service found male gender to be an independent risk factor for delirium, along with several other factors.11 Most studies of delirium have not reported gender as a major predictor.

Available studies on risk factors for delirium have not identified race as a specific predictor of delirium.
• Extremes of age.
• Male sex
• Pre-existing cognitive deficit e.g. dementia, stroke
• Severity of dementia
• Severe co-morbidity
• Previous episode of delirium
• Operative factors e.g. type of operation – hip fracture repairs are more likely to be associated with delirium as are emergency operations.
• Certain conditions – burns, AIDS, fractures, infection, low albumin, dehydration
• Drug use (implicated in nearly half of cases) and dependence e.g. benzodiazepines
• Substance misuse e.g. alcohol
• Extremes of sensory experience e.g. hypothermia or hyperthermia
• Visual or hearing problems
• Poor mobility
• Social isolation
• Stress
• Terminally ill
• Movement to a new environment
• ICU admission
High serum urea levels have also been found to be a risk factor for delirium in acutely admitted patients in one prospective study.15

• Acute infections
o Urinary tract infection
o Pneumonia
o Sepsis
o Viral infections
o Meningitis
o Encephalitis
o Cerebral abscess
o Malaria.
• Prescribed drugs
o Benzodiazepines
o Analgesics e.g. narcotics
o Anticholinergics
o Anticonvulsants
o Anti-parkinsonism medications
o Steroids.
• Toxic substances
o Substance misuse or withdrawal
o Alcohol – acute intoxication or withdrawal
o CO poisoning
o Exposure to heavy metals
o Barbiturate withdrawal.
• Vascular disorders
o Cerebrovascular haemorrhage or infarction
o Subdural haemorrhage
o Subarachnoid haemorrhage
o Vasculitis e.g. SLE
o Cerebral venous thrombosis
o Migraines.
• Metabolic causes
o Hypoxia
o Electrolyte abnormalities e.g. hyponatraemia and hypercalcaemia
o Hypo – or hyperglycaemia
o Hepatic impairment
o Renal impairment
o Cardiac failure or ischaemia.

• Vitamin deficiencies
o Thiamine deficiency
o Nicotininc acid deficiency
o Vitamin B12 deficiency.
• Endocrinopathies
o Hypo- and hyperthyroidism
o Hypopituitarism
o Hypo- or hyperparathyroidism
o Cushing’s disease
o Porphyria
o Carcinoid.
• Trauma
o Head injury.
• Epilepsy
o e.g. post-ictal.
• Neoplasia
o Primary cerebral malignancy
o Secondaries in the brain
o Paraneoplastic syndromes.
• Multiple aetiology
• Unknown aetiology

The commonest causes are medical conditions such as, infections, medications or drug withdrawal.

The diagnosis of acute confusional state is clinical. The following features may be present:

• Usually acute or subacute presentation.
• Fluctuating course.
• Consciousness is clouded.
• Impaired cognition.
• Disorientation.
• Poor attention.
• Memory deficits – predominantly poor short-term memory.
• Abnormalities of sleep-wake cycle including sleeping in the day.
• Abnormalities of perception e.g. hallucinations or illusions.
• Agitation.
• Emotional lability.
• Psychotic ideas are common but of short duration and of simple content.
• Neurological signs -e.g. unsteady gait and tremor.

Only some of these symptoms may be present. The symptoms may coincide with underlying dementia – which is common. The diagnosis is still clinical and marked by an acute deterioration.

The search for manifold causes of acute confusional state begins with a careful history taking emphasizing the patient’s condition before the onset of confusion. Patients are usually disoriented, so it is vital to take a history from a witness, either a relative or a carer.
The clinical examination should focus on
• Signs of diminished attentiveness
• Disorientation
• Drowsiness
• Any localizing neurological sign
• Other clues to the cause (eg. Pyrexia, signs of meningeal irritation)
From the clinical data the clinician is directed to the appropriate laboratory investigations.
Often, even after all diagnostic tests are completed, one may still not know the cause of a confusional state. The proper approach is to observe the patient in the hospital for a number of days under stable conditions. New clues may appear or an obscure confusion perhaps related to a medication, may clear up, while other causes such as renal or hepatic failure may worsen and lead to coma.1

Patients presenting with an acute confusional state should be evaluated first with a careful history, taken from a reliable person who knows the patient well (if possible), and a physical examination. The history should include details of prior illnesses, a complete medication list, and a historical baseline level of function. It also should include the temporal course of the changes in mental status.
• The context of the syndrome is especially important—the location of the patient when the condition was first noticed, eg, the intensive care unit, nursing home, or psychiatric ward.

• Underlying or past medical conditions such as diabetes, hypertension, and prior strokes should be documented.

• The historian should ascertain whether the patient has suffered confusional episodes before and whether he or she recovered. Preexisting cognitive deficits or dementia are potent risk factors for the development of delirium in association with illness, hospitalization, or surgery.

• The features of confusion should be elucidated. Is the patient wakeful and alert, or sleepy; agitated, or calm; aphasic, or with normal language and speech?

• Alcohol and substance abuse history should be documented.

• All medications currently being administered to the patient should be reviewed, as well as reconciliation with home medications. Withdrawal from sedative or hypnotic drugs such as benzodiazepines can mimic alcohol withdrawal or delirium tremens.

• If the patient is unable to communicate verbally, the examiner should evaluate whether he or she can communicate with eye blinking and vertical eye movements (ie, locked-in syndrome). The examiner should also look for evidence of subtle seizures, such as eye blinks, facial twitches, or automatisms.

• The physician must also look for signs such as fever, confusion, and seizures (as in herpes encephalitis), or stiff neck and fever (as in meningitis or subarachnoid hemorrhage). These are true medical emergencies.

The examination should be complete enough to consider diseases of virtually any organ system. The neurologic examination should look especially at disorders of higher function, such as aphasia or neglect. Other focal neurologic findings such as eye movement and other cranial nerve abnormalities, motor, sensory, and cerebellar findings should be noted.
• Examine the general behavior and comment on level of arousal, alertness, and agitation.

• Patients with delirium, in addition to their “negative” symptoms and signs of deficient cognitive functions, have “positive” symptoms such as agitation, restlessness and hyperactivity, delusional thinking, hallucinations, and anxiety.

• Patients with delirium, unlike those with dementia, frequently have autonomic abnormalities such as tachycardia, hypertension, fever, sweating, and piloerection.

• Examine vital signs, neck stiffness, airflow, lungs, heart, and any abnormal movements such as tremor, myoclonus, tonic-clonic activity, or asterixis.

• Specific neurologic signs should also be sought carefully. These include a detailed examination of higher functions; because the higher functions examination is hierarchical, wakefulness and arousal should be tested first.

• Language should be tested carefully, including the ability to name, repeat, comprehend, read, write, and utter spontaneous speech. Aphasia is frequently mistaken for confusion by emergency department staff.

• Hemispatial attention should be checked (attention to left side is abnormal in focal disorders of right hemisphere) by asking the patient to draw, point to people in the room, or read. If not specifically sought, the neglect syndrome will be missed.

• Look for subtle movements of the face or eyes that are indicative of seizures.

• Eye movements to command should be checked if the patient appears unable to communicate (ie, locked-in syndrome).

• Extinction with double simultaneous stimulation (visual, auditory, tactile, or somatosensory) may be features of the neglect syndrome. Assess whether the patient can recognize his or her illness. Anosognosia is defined as the denial or neglect of illness, commonly occurring after right hemisphere injuries.

• The cranial nerve, motor, sensory, and cerebellar examinations should be geared toward discovering other neurologic signs that can help with localization or uncover an underlying condition. Specific examples of examination findings and their significance follow:

• The cranial nerve examination should include funduscopic examination. Subhyaloid hemorrhages may be seen in cases of subarachnoid hemorrhage or trauma, and papilledema or absent venous pulsations may indicate increased intracranial pressure.

• The visual fields should be checked with finger counting or response to threat, to discover subtle visual field defects or visual neglect/extinction.

• Facial symmetry usually can be assessed, as can gag reflex. A swallow test may be needed to determine if the patient can handle oral food or medication.

• Motor examination may show a subtle hemiparesis (eg, pronator drift, subtle proximal or distal unilateral weakness).

• Focal long-tract signs (eg, hyperreflexia, Babinski sign), unilateral dyscoordination (ie, cerebellar lesion), and crossed sensory findings (eg, Brown-Sequard syndrome, brainstem lesion) can be the key to diagnosis of a focal lesion.

• Evaluating whether the patient can walk is crucial. Cerebellar hemorrhages and infarctions may be missed unless gait testing is performed.
Delirium is commonly mistaken for the following diagnoses
• Dementia – for example, Lewy body type dementia which typically has a fluctuating course also.
• Depression.
• Bipolar disorder.
• Functional psychoses e.g. schizophrenia.

Distinguishing dementia from an acute confusional state is a great problem, specially in the elderly, since the two may coexist if a fever, other medical problem, or a poorly tolerated medication supervenes in a mildly demented patient, producing a so-called beclouded dementia. The memory loss of dementia brings about a confusional state that varies little in severity from hour to hour and day to day. Poor mental performance is derived mainly from incomplete recollection, inadequate access to names and ideas and the inability to retain new information thus affecting orientation and factual knowledge.
In contrast to the acute confusional state, attention, alertness and coherence are preserved until the most advanced stages. Eventually dementia produces a chronic confusion with breakdown of all types of mental performance, and the distinction from an acute encephalopathy depends mainly on the longstanding nature of the condition.

These should be guided by the clinical presentations and are aimed at identifying an underlying cause of acute confusional state. Typical investigations that can be performed include16
First Line Other Useful Tests
Blood Tests Full blood count, ESR
Urea and electrolytes
Calcium, magnesium
Liver function tests
Thyroid function tests Cardiac enzymes
Protein electrophoresis
Vitamin B12
Copper studies
Syphilis serology
Antinuclear antibody (ANA), anti-double-stranded DNA (anti-dsDNA), antithyroid antibodies
Tumour markers, prostate-specific antigen
CNS Investigations Head imaging (CT and/or MRI) Lumbar puncture
Other Arterial blood gases
Infection screen (blood cultures, chest X-ray, urine culture)
Toxicology screen of blood and urine Viral screen, ads appropriate (e.g. consider HIV)
Urinary porphyrins

• Neuroimaging –
The availability of CT scan and MRI has focused attention on the cause of acute confusional state that are radiologically detectable like – haemorrhage, infarcts, tumours or hydrocephalus.

• EEG –
EEG can help diagnose seizures, hepatic encephalopathy, and focality due to stroke, and it can help differentiate psychiatric from organic disease (EEG findings are normal in virtually all purely psychiatric disorders).10

• Toxicological Analysis of Blood and Urine –
It is necessary in any case of acute confusional state where the diagnosis is not immediately clear. However the presence of exogenous drugs and toxins, specially alcohol, does not exclude the possibility that other factors, particularly head traumas are also contributing to the clinical state.

• Lumbar Puncture and CSF Study –
Lumbar puncture should be performed if CT scan findings are negative and neurologic infection (e.g. meningitis, encephalitis) is suspected.
The CSF should be sent for protein, glucose, cytology, Gram stain and culture.

The management involves –
1. Identifying the cause and correcting it if possible, like – correction of metabolic abnormalities, treatment of infection.
2. All unnecessary medication should be stopped.
The management can be divided in to
1. Supportive management including dietary measures
2. Environmental measures
3. Medical management
4. Management post-discharge.

Supportive management
• Clear communication.
• Reminders of the day, time, location and identification of surrounding persons.
• Have a clock available.
• Have familiar objects from home around patients especially glasses, walking aids and hearing aids.
• Staff consistency – both doctors and nurses.
• Relaxation e.g. watch television.
• Involve family and carers.
• Diet –
 Dietary consultation may be needed if liver disease is present or if the patient is malnourished, requires nasogastric feeding, or is chronically malnourished because of living alone. A calorie count may be indicated.
 If the patient is diabetic or has hepatic encephalopathy, restriction of sugar and calories, or protein, respectively, is indicated.
 Patients with chronic weight loss due to alcoholic/nutritional or degenerative dementia may require caloric supplements.

Environmental measures
• Adequate space
• Single rooms if possible
• Avoid speciality jargon
• Control noise
• Control room lighting
• Control room temperature.
Medical Management
In general, a specific diagnosis must be made before selecting a medication to be used; however, treatment must begin while awaiting the results of studies, even in the absence of a diagnosis. On arrival to the ED, administration of thiamine and glucose, followed by naloxone and flumazenil, is important. Empiric antibiotics can be given if an infection is suspected. Acyclovir should be administered if the physician has any suspicion of herpes encephalitis, because early treatment can prevent long-term neurologic damage. The diagnosis of herpes encephalitis by polymerase chain reaction (PCR), or even by EEG or MRI, can be done later. Most other medications depend upon the diagnosis.
Thiamine, naloxone, flumazenil, glucose, and acyclovir are used to reverse coma due to treatable causes, including Wernicke-Korsakoff syndrome, opiate intoxication, benzodiazepine intoxication, and herpes encephalitis, respectively.
During the period of confusion, sedative drugs are best avoided, as they may exacerbate the confusion, although occasionally drugs such as haloperitol (1-10 mg 8 hourly) may be required.
In delirium tremens (alcohol withdrawal), the treatment is a tapered course of diazepam with high dose intravenous thiamin.

Management post-discharge
• The symptoms of delirium last longer than the underlying condition.
• This means that patients are discharged with persisting abnormalities.
• These abnormalities include disorientation, inattention and depression.
• Families and carers may also need to be supported and given advice and reassurance.

Drug induced delirium is very common amongst the elderly. Drugs can be the sole cause of delirium in some. Common drug causes of delirium include:
• Benzodiazepines
• Narcotic analgesics
• First generation antihistamines
• Antispasmodics
• Flouroquinolones
• Warfarin
• Captopril
• Theophylline
• Isosorbide dinitrate
• Dipyridamole
• Frusemide
• Lithium
• Tricyclic antidepressants
• Cimetidine
• Antiarrhythmics
• Digoxin
• Steroids
• Beta blockers
• Over the counter medications e.g. liquid medications containing alcohol, chlorpheniramine.
The role of medications may be suggested by a temporal relationship between onset of delirium and start of new medication. However, this is not always the case and practitioners need to be aware of this. Medication lists should be thoroughly reviewed in delirium. The exact mechanism of delirium is unclear but it is postulated that central cholinergic pathway blockade is a major factor.10 This may explain why anticholinergic medications readily lead to delirious states. It may be that this factor along with the pharmacokinetic changes that occur later in life and co-morbidities increase the susceptibility of elderly patients to drug induced delirium.

Management involves stopping the offending drug – however, the actual causal medication is often unknown. In this case all unnecessary medications should be stopped or doses reduced. These medications can be increased or re-introduced when the patient has improved. Furthermore, it may be prudent to prescribe alternatives to medications with high anticholinergic activity e.g. proton pump inhibitors rather than cimetidine.


1. Infections e.g. clostridium difficile and methicillin-resistant staphylococcus aureus.

2. Pressure sores.

3. Fractures e.g. femoral or hip fractures from falls.

4. Residual psychiatric and cognitive impairment.

5. Some progress to stupor, coma and eventual death.

The prognosis of confusional states is highly variable. Patients frequently become much better than the expected recovery predicted by the admitting physicians. The prognosis may depend on general medical care and attention, rather than specific management of the encephalopathy. Many patients with confusional episodes recover completely. Unfortunately, some patients are left with chronic neurocognitive deficits.
The mortality rate in elderly hospitalised patients in the US is estimated at 22 – 76%.8 Some patients may not recover for months. Many patients become institutionalized after delirium. In fact a prospective cohort study in Canada discovered that symptoms of delirium persist for up to a year after an episode.18 Furthermore, the same study revealed that there was a worse prognosis if the episode has a protracted in-patient course. Patients with malignancy or HIV also have a worse prognosis.8

Education of the family is a key part of the management of the delirious patient. If the prognosis is not good, the family may or may not reconcile themselves to this. Family meetings and tactful presentations of the patient’s condition and prognosis may help. If the physician is unsure about the prognosis, neurologic, neuropsychologic, or other appropriate consultation may be made to assist in family education. If the patient clearly has little chance of returning home or caring for his or her own needs independently, the family should be presented tactfully and compassionately with this information.




To identify the aetiology of Acute Confusional State among the hospitalized patients in Dhaka Medical College Hospital.


1.To identify the percentage of patients admitted with Acute Confusional state by the type of acute illness.

2. To identify the aetiology of Acute Confusional State in different age & sex groups.

3. To determine the proportion of patients admitted with acute confusional state among the total admitted patients.


A prospective study was conducted at DMCH to evaluate etiology of patients admitted with a provisional diagnosis of acute confusional state.

The study was conducted in medicine unit-blue at DMCH, Dhaka. This medicine unit was selected randomly from the existing 5 medicine units of DMCH.

The study spanned over the period of four months from July 08 to October 08.

All adult patients of both gender admitted with a provisional diagnosis of acute confusional state in medicine unit blue of DMCH during this study period fulfilling the inclusion criteria were included in the study.

A total number of 345 cases with age ranging from 16 to 93 years were purposefully collected for conducting the study.

Patients were assessed on the basis of the definition of acute confusional state given by the Diagnostic and Statistical Manual, 4th Edition (DSM-IV) of American Psychiatric Association (APA) and level of consciousness was assessed according to Glasgow Coma Scale. Detailed neurological and systemic examination was done. All the relevant investigations like complete blood count, random blood sugar, blood urea, serum creatinine, serum electrolytes, prothrombin time, urine RE, chest X-Ray were done immediately as per clinical context. Other important investigations like lumbar puncture, CT scan head, MRI, Toxicologic screening etc were done where indicated.

All the necessary information was collected in a standardized data sheet by interviewing patient’s attendants and from hospital records. Finally all the necessary data were processed, analyzed by using SPSS programme, presented in tables and diagrams and conclusion was drawn. The study result was compared with some recognized international studies.


Patients admitted with some of the following features of acute confusional state in medicine unit blue in Dhaka Medical college hospital were included in the study –
• Usually acute or subacute presentation (onset within 24-72 hours).
• Fluctuating course.
• Consciousness is clouded.
• Disorientation.
• Memory deficits – predominantly poor short-term memory.
• Abnormalities of sleep-wake cycle including sleeping in the day.
• Abnormalities of perception e.g. hallucinations or illusions.
• Agitation.
• Emotional lability.
• Psychotic ideas are common but of short duration and of simple content.
• Neurological signs -e.g. unsteady gait and tremor.


o Patients known to have previous history of stroke, chronic degenerative neurological disease where cognitive function is impaired will be excluded from this study.

o Patients admitted in departments other than medicine will not be enrolled in this study.


All information was collected from patients’ attendants and hospital records. No intervention was done on study purpose. Written consent was taken from the patients’ attendant.


Table 1: proportion of patients admitted with acute confusional state among the total admitted patients:

Total no. of admitted patients No. of patients with acute confusional state Percentage (%)
Male Ward 1112 239 21.49
Female Ward 537 106 19.74
Total 1649 345 20.92

Figure 1: Proportion of male patients with acute confusional state (n=239/1112)

Figure 2: Proportion of female patients with acute confusional state

Figure 3: Proportion of patients admitted with acute confusional state among the total admitted patients (n=345/1649)

Table -2: Aetiological classification of study population presented with acute confusional state (n=345):

Aetiology Total Percentage %
stroke 86 24.92
Acute poisoning 76 22.03
Hepatic encephalopathy 41 11.88
Electrolyte imbalance 32 9.28
CNS infection 25 7.24
Systemic infection 14 4.05
Hypoxia 15 4.35
Disturbance of glucose metabolism 13 3.77
Uraemia 5 1.45
Unknown aetiology 24 6.96
Multiple aetiology 7 2.03
Other 7 2.03
Total 345 100%

Figure 4: Proportion of different aetiology of acute confusional state:

Table 3: Distribution of study population according to age group (n=345):

Age group (years) Total no. of patients percentage
16-25 77 22.32
26-35 48 13.91
36-45 38 11.01
46-55 46 13.33
56-65 63 18.26
66-75 52 15.07
76-85 16 4.64
>85 5 1.44
Total 345 100%

Figure 5: Age distribution of study population

Table 4: Distribution of study population according to sex (n=345)

Aetiology Male Percentage
(n=239) Female Percentage
stroke 57 23.75 29 27
Acute poisoning 52 21.67 24 22.43
Hepatic encephalopathy 30 12.5 11 10.28
Electrolyte imbalance 22 9.16 10 9.34
CNS infection 17 7.08 8 7.47
Systemic infection 10 4.16 4 3.73
Hypoxia 14 5.83 1 1
Disturbance of glucose metabolism 9 3.75 4 3.74
Uraemia 4 1.67 1 1
Unknown aetiology 15 6.25 9 8.4
Multiple aetiology 5 2.08 2 1.87
Other 4 1.67 3 2.8
Total 239 100% 106 100%

Figure 6: Sex distribution of study population (n=345)

Table 5: Broad aetiological classification of acute confusional state of study population (n=345)

Types No. of patients Percentage (%)
Metabolic cause (including poisoning) 182 52.75
Organic cause 132 38.26
Unknown cause 24 6.95
Multiple cause 7 2.02
Total 345 100%

Figure 7: Broad aetiological classification of acute confusional state

Table 6: Age and sex distribution of study population presented with acute confusional state due to stroke (n=85):

Age (years) Male Female Total no. Percentage(%)
26-35 ¬¬¬¬¬¬¬¬¬¬ ——- 1 1 1.17
36-45 4 5 9 10.58
46-55 7 3 10 11.76
56-65 14 10 24 28.23
66-75 19 9 28 32.94
76-85 8 1 9 10.58
>85 4 ——- 4 4.71
Total 56 29 85 100%

Figure-8: sex distribution of study population presented with acute confusional state due to stroke (n=85):

Table 7: Aetiological classification of study population presented with acute confusional state due to acute poisoning (n=76):

Aetiology Male Female Total Percentage
Unknown 23 13 36 47.36
Insecticides(OPC) 22 8 30 39.47
Sedetive/ Hypnotics 7 3 10 13.15
Total 52 24 76 100%

Table 8: Age and sex distribution of study population presented with acute confusional state due to acute poisoning (n=76):

Age group Unknown OPC Sedative Total Percentage
Male Female Male Female Male Female
16-25 8 10 15 8 5 2 48 63.15
26-35 10 2 3 —- 2 1 18 23.68
36-45 3 —- 3 —- —- —- 6 7.89
46-55 1 1 —- —- —- —- 2 2.63
56-65 1 —- 1 —- —- —- 2 2.63
> 66 —- —- —- —- —- —- —- —–
Total 23 13 22 8 7 3 76 100%

Table 9: Aetiological classification and sex distribution of study population presented with acute confusional state due to hepatic encephalopathy (n=41):

Aetiology Male Female Total Percentage
Decompensated CLD 25 7 32 78.05
Fulminant Hepatic Failure 3 4 7 17.07
Multiple Liver Abscess 1 ——- 1 2.44
Hepatocellular carcinoma 1 ——– 1 2.44
Total 30 11 41 100%

Table 10: Age distribution of study population presented with acute confusional state due to hepatic encephalopathy (n=41):

Age group Total Percentage
16-25 8 19.51
26-35 14 34.14
36-45 6 14.63
46-55 9 21.95
56-65 3 7.31
> 66 1 2.44
Total 41 100%

Table 11: Age & Sex distribution of study population presented with acute confusional state due to electrolyte imbalance (n=32)

Age Group(years) Male Female Total Percentage
16-25 3 1 4 12.5
26-35 3 1 4 12.5
36-45 4 1 5 15.63
46-55 3 1 4 12.5
56-65 3 3 6 18.75
66-75 5 2 7 21.87
76-85 1 —- 1 3.13
>85 —- 1 1 3.13
Total 22 10 32 100%

Table 12: Aetiological classification of study population presented with acute confusional state due to CNS infection (n=25):

Aetiology Male Female Total Percentage
Viral meningitis 2 —- 2 8
Pyogenic meningitis 1 1 2 8
Tubercular meningitis 2 —- 2 8
Meningo-encephalitis 5 2 7 28
Encephalitis 7 4 11 44
Brain Abscess —- 1 1 4
Total 17 8 25 100%

Table 13: Age distribution of study population presented with acute confusional state due to CNS infection (n=25):

Age group(years) Meningitis Meningo-encephalitis Encephalitis Brain Abscess Total Percentage
16-25 —- 2 6 —- 8 32
26-35 3 2 2 1 8 32
36-45 1 —- 2 —- 3 12
46-55 —- —- —- —- —- —-
56-65 1 3 —- —- 4 16
66-75 —- —- 1 —- 1 4
76-85 —- —- —- —- 1 4
>85 —- —- —- —- —- —-
Total 5 7 11 1 25 100%

Table 14: Sex distribution of study population presented with acute confusional state due to CNS infection (n=25):

Aetiology Male Female Total
Meningitis 5 1 6
Meningo-encephalitis 5 2 7
Encephalitis 7 4 11
Brain Abscess —- 1 1
Total 17 8 25

Table 15: Aetiology and Sex distribution of study population presented with acute confusional state due to systemic infection (n=14):

Aetiology Male Female Total Percentage
Pneumonia 2 1 3 21.42
UTI 3 —- 3 21.42
Septicaemia 2 —- 2 14.28
PUO 2 3 5 35.71
Cerebral Malaria 1 —- 1 7.14
Total 10 4 14 100%

Table 16: Age distribution of study population presented with acute confusional state due to systemic infection (n=14):

Age group(years) Total Percentage
16-25 1 7.14
26-35 —- —-
36-45 1 7.14
46-55 1 7.14
56-65 6 42.85
66-75 5 35.71
>75 —- —-
Total 14 100%

Table 17: Aetiology and Sex distribution of study population presented with acute confusional state due to hypoxia (n=15):

Aetiology Male Female Total Percentage
Respiratory failure 10 1 11 73.33
Cor pulmonale 4 —- 4 26.66
Total 14 1 15 100%

Table 18: Age distribution of study population presented with acute confusional state due to hypoxia (n=15):

Age groups(years) Respiratory Failure Cor Pulmonale Total Percentage
16-25 —- —- —- —-
26-35 1 —- 1 6.66
36-45 —- 1 1 6.66
46-55 3 2 5 33.33
56-65 3 1 4 26.66
66-75 2 —- 2 13.33
>75 2 —- 2 13.33
Total 11 4 15 100%

Table 19: Aetiology and Sex distribution of study population presented with acute confusional state due to disturbance of glucose metabolism (n=13):

Aetiology Male Female Total Percentage
Diabetic Ketoacidosis 5 3 8 61.54
HONK 2 —- 2 15.38
Hypoglycemic coma 2 1 3 23.07
Total 9 4 13 100%

Table 20: Age distribution of study population presented with acute confusional state due to disturbance of glucose metabolism (n=13):

Age Groups (years) Total Percentage
16-25 1 7.69
26-35 —- —-
36-45 2 15.38
46-55 7 53.85
56-65 2 15.38
66-75 1 7.69
76-85 —- —-
>85 —- —-
Total 13 100%

Table 21: Age and Sex distribution of study population presented with acute confusional state due to unknown cause (n=24):

Age Groups(years) Male Female Total Percentage
16-25 3 —- 3 12.5
26-35 —- —- —- —-
36-45 1 —- 1 4.16
46-55 2 2 4 16.66
56-65 5 3 8 33.33
66-75 3 3 6 25
76-85 1 1 2 8.33
>85 —- —- —- —-
Total 15 9 24 100%

Table 22: Aetiology and Sex distribution of study population presented with acute confusional state due to other causes (n=7):

Aetiology Male Female Total Percentage
Hypertensive Encephalopathy 1 1 2 28.57
ICSOL 2 —- 2 28.57
Post ictal 1 —- 1 14.28
Post partum encephalopathy —- 1 1 14.28
CNS lupus —- 1 1 14.28
Total 4 3 7 100%


During the period of July, 2008 to October, 2008 total 25 admissions occurred in medicine unit blue of DMCH. In male ward, a total number of 1112 patients were admitted during these four month period. Among them 239 patients presented with the features of acute confusional state due to different aetiology fulfilling the inclusion criteria of current study, which constitute about 22% of total admission in male ward (Table-1, Fig-1). In female ward, among 537 total admitted patients, 106 were in acute confusional state, which is about 20% of total admission in female ward (Table-1, Fig-2). So a total number of 1649 patients were admitted in both male and female wards, among them patient with acute confusional state was 345. It is 21 percent of total admission (Table-1, Fig-3). It is almost consistent with international data, which says, acute confusional state occurs in about 15-20% of all general admissions to hospital.9 ¬

Regarding the aetiology of different cases of acute confusional state, (Table-2, Fig-4) stroke topped the list (25%). It was followed by acute poisoning (22%), hepatic encephalopathy (12%), electrolyte imbalance (9.28%), CNS infection (7.24%), unknown (7%), systemic infection (4%), disorders of glucose metabolism (4%), other (2%), multiple aetiology (2%) and uraemia (1.45%). It is interesting to note that despite good clinical history, examination and laboratory investigations exact aetiology of acute confusional state of a good number of patients remained unknown, constituting 7% of total study population.

There was considerable variation in the age distribution (Table-3, Fig-5) of the study population. Age range was 16-93 years. Majority of the patients were in the age group of 16-25 years (22.32%). Next common age group was 56-65 years (18.26%). This finding reflects one of the important risk factors of acute confusional state which is extremes of age. Though from the international studies, it was thought that, acute confusional state is predominantly a state of the elderly, but in this current study, younger age group constituted the highest percentage. It may be due to the large number of acute poisoning cases in the current study; 16-25 years age group is the principal victim of the acute poisoning. Another reason may be total lifespan which is less in our population than in western population.

Acute confusional state due to stroke, electrolyte imbalance (eg-hyponatraemia), systemic infection (eg-pneumonia, UTI) was common in the older age group. On the other hand, acute poisoning, CNS infection, hepatic encephalopathy were common aetiology of younger age group.

Regarding gender distribution it was found that among total 345 patients with acute confusional state, number of male patients was 239, which constitute 69.27% and number of female patient was 106, constituting 31% (Fig-6).

This finding is similar to a study of Higashi et al. 20, which showed the percentage of male was 68.18% and female was 31.82%. This finding reflects that male sex is an independent risk factor for acute confusional state. However, as in our hospital, total number of bed allocated for male patient is more than female patient, so such a high percentage of male patient in comparison to female counterpart may not be the true reflection of the scenario.

In this study,53%of patients with acute confusional state was due to metabolic causes and 38% was due to organic causes(Table-5,fig-7). Unknown cause and multiple cause constitute the remainder 9%. This finding is consistent with a studu by Plum & Posner21 ,who showed 65.2% cases due to metabolic and 34.8% due to organic causes. Another study by Faheemur Rehman Khan et al 22showed that neurological lesions and metabolic encephalopathies accounted for about 70% of the cases, followed by infections(10%) and drugs/ toxins (8%).

In this study, the most frequent cause of acute confusional state is found to be stroke, comprising 25% of total study population (Table-1). This is similar with an international study23. In the study by Levy et al24 36.2% of non traumatic acute confusional patients were due to stroke. Present study is almost similar with that study.

In this study, the incidence, of stroke with altered level of consciousness was highest in the age group 56-75 years (61.2%) (Table 6). A study by a H Henon25 showed acute confusional state occurs in 1/4th of stroke patients older than 40 years.

The incidence of stroke causing acute confusional state was 65.88% in male and 34.11% in female (Fig-8). Dalal et al26 showed 67% in male and 33% in female which is similar with this study.

The male preponderance in the present study may be due to socio-cultural and religious stigmata prevailing in our society for which female are not generally brought to the hospital. Female bed allocation is less than the male in our hospital, so naturally number of female patient is less (almost half) than male patient in the study population.

Next to stroke the second most common cause of acute confusional state was found to be acute poisoning, comprising 22% of total cases (Table-2) and 42% of metabolic cases. Plum and Posner21 showed 29.8% altered consciousness were due to drug poisoning and 37.5% of altered consciousness of metabolic causes was due to acute poisoning.

The poisonous substances used for poisoning (Table-7) were mostly unknown (47.36%), followed by insecticides (39.47%) and sedatives/hypnotics (13.15%). The patients of unknown poisoning are mainly travelers. They are victims of street poisoning, which are usually strong hypnotics or mixture of two or more drug that can induce deep sedation. These patients usually revive safely within 24-48 hours. The high percentage of poisoning by unknown substances reflects the lack of availability of toxicological analyzing facilities in our country.

Second important cause of poisoning was insecticides like organo phosphorus compounds (39.47%). In one study led by Azhar MA et al27 12.7% cases of poisoning causing acute confusional state were found to be due to OPC. It might be due to easy availability of this poison in the rural areas at a quite cheaper rate. Insecticides were taken by the patients coming from poor social classes of rural areas. On the contrary sedatives and anti- depressants were commonly used drug for poisoning by higher social classes.

No case of alcohol intoxication was found in this study which may be due to limited number of study case or majority of study population belonging to poor socio- economic status. However alcoholism is not very uncommon in our country nowadays.

Majority of poisoning cases were found in the age group of 16-25 years (63.15%) (Table-8). Helliwell et al28 also found in their study that majority of the poisoning patients in the age group 20-29 years (33.9%). These young patients usually took poisons or over dose of drugs intentionally, often impulsively after a disagreement with a key person in their family. Most of these patients had no wish to die. They deliberately took poison to teach others a lesson or to manipulate them into an attitude or course of action they would otherwise reject29.

Next to stroke and acute poisoning, third common cause of acute confusional state was found to be hepatic encephalopathy (12%) (Table 2). This is nearly consistent with the study by Levy et al24 in which 10.2% of altered consciousness was due to hepatic encephalopathy. Decompensated CLD was found as the commonest precipitating factor in 78.05% of cases(Table-9). Next was fulminant hepatic failure (17.07%). The peak age group in the present series was 26 to 35 years (34.14%) (Table -10 ).

Regarding sex distribution, it was interesting to note that hepatic encephalopathy due to CLD was more common in male (male : female =3.5:1) but fulminant hepatic failure was more common in female (male : female = 0.75 : 1) (Table-9). It may be due to the fact that female are more prone to develop hepatic encephalopathy due to hepatitis E virus infection during their pregnancy or post partum period.

In this study, out of 345 cases, 32 cases (9.28%) were due to electrolyte imbalance (hyponatraemia) (Table – 2). Hyponatraemia has been detected as the most frequent electrolyte disorder in clinical medicine30. Mild hyponatraemia is seldom associated with any specific features and symptoms usually relate to the underlying cause31. Severity of symptoms depends on the rate of fall of plasma sodium concentration as well as absolute value32. A patient with hyponatraemia may present with clouding of consciousness including coma.

The highest prevalence of electrolyte imbalance was in the age group of 56 to 75 years (40.63%) (Table -11). Kugler and Hustead33 showed in a study that elderly people are more susceptible to develop water and electrolyte imbalance including hyponatraemia. Again prevalence of many diseases responsible for hyponatraemia increases with age.

Next important cause of acute confusional state was found to be CNS infection (7.24%) (Table -2). Among CNS infection causing acute confusional state, encephalitis is the most frequent cause (44%) followed by meningo-encephalitis (28%), meningitis (24%) and brain abscess (4%) (Table – 12). In this study majority of the patients with CNS infection was found to be in the younger age group of 16 to 35 years (64%) (Table -13 ).

On the contrary, systemic infection causing acute confusional state was more common in older age group, 56 to 75 years (78.57%) (Table – 16). Systemic infections causing altered consciousness were found to be pneumonia (21.42%), UTI (21.42%), septicaemia (14.28%), PUO (35.71%) and cerebral malaria (7.14%) (Table -15).

15 cases of acute confusional state was found to be due to hypoxia (4.35%) (Table – 2) with or without hypercapnia. Hypoxia was due to respiratory failure (73.33%) and cor pulmonale (26.66%) (Table -17). Male : female was found to be 14 : 1 (Table-16), reflecting that respiratory failure and cor pulmonale are predominantly occurring in male patients. This may be due to the fact that our female population are usually non-smokers so they are less prone to develop COPD, which was the basic diagnosis of patients of acute confusional state due to hypoxia. The predominant age group was 46 to 55 years (33.33%)(Table-18) reflecting it is mainly a disease of middle aged male patient.

In this study 13 cases (3.77%) of acute confusional state was found to be due to disturbance of glucose metabolism (Table – 2) in the form of diabetic ketoacidosis (61.54%), hypoglycaemic coma (23.07%) and HONK (15.38%) (Table – 19). In the study of Helliwell et al28 2% cases of altered consciousness were due to DKA. In another study of Boston City Hospital, Solman and Aring34 found 1.7% due to diabetic coma. These two studies are consistent with this study as because here 5 cases out of 345 cases were due to DKA which is 1.45% of total study population.Peak incidence of age was in 46-55 years (54%) (Table – 20).

Acute confusional state due to uraemia was found in 1.45% of cases (Table-2). As there is separate department of nephrology, this findig may be lower than the real picture.

The aetiology of acute confusional state of study population remained unknown in 7% cases, multiple in 2% cases and other in 2% cases (Table-2). Unknown aetiology predominated in the elderly population, age group 56 to 75 years (58.33%) (Table -21). Many of these patients might have multiple pathology.

Among 7 other causes there was 2 cases of hypertensive encephalopathy, 2 cases of ICSOL, 1 post ictal encephalopathy, 1 post partum encephalopathy and 1 CNS lupus(Table-22). These diversity of aetiology emphasize the fact that rare or uncommon causes of acute confusional state should also be kept in mind while dealing with a patient with altered level of consciousness. Sometimes this may be life saving for the patient and very much rewarding for the physician.


In this prospective hospital based study, 345 adult patients presenting with acute confusional state were collected from medicine unit-blue of Dhaka Medical College Hospital during the period of July’08 to October’08. Patients known to have previous history of stroke, chronic dementing neurological disease were excluded from the study. Patients admitted in departments other than medicine were not enrolled in this study. The preliminary history, physical findings and some routine and special investigations helped to reach a diagnosis.

This study revealed that, patients with acute confusional state constitute about 21% of total hospital admission in medicine wards.

From this study, peak incidence of acute confusional state was found to be in two age groups: one in 2nd to 3rd decades and another in 5th to 6th decades.The first peak was due to acute poisoning, CNS infection and hepatic encephalopathy; and the second peak was due to stroke,electrolyte imbalance, systemic infection and disturbance of glucose metabolism.

This study also showed male preponderance over female and metabolic causes higher than the structural causes.

Stroke comprised the highest percentage (25%) of cases in this series. Incidence of stroke was highest in 5th to 7th decades (61%). Males were affected more than the females.

Second common cause of acute confusional state was acute poisoning (22%), mostly due to unknown poisoning (47%) and insecticides (39.5%).Peak incidence was in 2nd to 3rd decades (63%).

Third common cause of acute confusional state was found to be hepatic encephalopathy (12%), predominantly due to decompensated chronic liver disease (78%). Peak age group was 2nd to 3rd decades (34%).

Electrolyte imbalance comprised 9.28% cases and was due to hyponatraemia. Peak incidence was in 5th to 7th decades (41%).

CNS infection was found in 7.24% of cases, of which 44% was encephalitis, followed by meningo-encephalitis (28%). Majority was found in the younger age group of 2nd to 4th decades (64%). On the contrary, systemic infections, comprising 4% of acute confusional state of the study population, was found to be more common in older age group of 5th to 7th decades (78.6%).

Hypoxia comprised 4.35% cases, which was due to respiratory failure(73%) and cor pulmonale (27%). Male, female ratio was 14:1. Predominant age group was 46-55 years (33%).

In this study,3.77% patients of acute confusional state were due to disturbance of glucose metabolism, mostly due to diabetic keto-acidosis (61.5%). Peak incidence was in the age group of 46 – 55 years (54%).

The remaining cases of this study had acute confusional statedue to uraemia (1.45%), multiple aetiology (2%), some other specific less common aetiology (2%) and unknown aetiology(7%).


1. The present study is based on patients of medicine indoors of DMCH which may not be true representative of the whole community.

2. The study population is small.

3. Total time span is also limited.

4. Patients admitted in departments other than medicine were excluded from the study. So acute confusional state due to post operative complications or head injury could not be enrolled in this study.

5. In our hospital total number of bed allocated for female patients is much less than for male patients. So naturally female sample size was always less than male sample size. So gender distribution of different aetiology of acute confusional state may not represent the actual scenario prevailing in our community.


The study was designed to work out the important aetiology and epidemiology of acute confusional state in our population, so as to help in pointing out important and common causes with age and sex distribution of acute confusional state in our set up, thus helping to keep in mind different diseases while we are confronted with a patient of acute confusional state. This prospective hospital based study with a limited number of study population may not reflect the exact situation of the condition in the community, but its nearness to the reality cannot be underestimated. Maximum effort was given to find out the cause of acute confusional state by thorough evaluation of its clinical aspects and correlating them with the laboratory findings.

Age is an important predictor of the aetiology of acute confusional state. In older age group acute confusional state is mostly due to stroke, electrolytic imbalance, systemic infection or disturbance of glucose metabolism. In younger age group, acute poisoning, CNS infection or hepatic encephalopathy are the common aetiology of acute confusional state. It is important to note that, many causes of altered consciousness are completely reversible with prompt diagnosis and proper management, like- infections & metabolic abnormalities. This finding emphasize the great importance of early accurate diagnosis of acute confusional state, as correct diagnosis can lead to judicious management and save many valuable lives.

The study also highlighted that the aetiology of a significant number of cases of acute confusional state remained unknown. So in conclusion, it needs to be mentioned that, our clinical and investigation facilities must be improved a lot to solve the unresolved factors of the present study, which would improve the morbidity and mortality from acute confusional state.



Md. Shah Alam, 55 years of age, smoker, shop keeper, hailing from comilla admitted in medicine unit-blue, DMCH on 24th July, 2008 with the history of repeated vomiting for 6-7 times in last 6 hours, altered level of consciousness for 4 hours and weakness of left side of his body for 2 hours. There was a single episode of convulsion 2 hours ago. He had no history of headache or fever. He was hypertensive for last 5years with irregular medications. He was not a known case of diabetes. His father was hypertensive and died of stroke. He was smoker with 25 pack year smoking history. He was non alcoholic.

On admission he was drowsy with normal pupil reaction. Signs of meningeal irritation was absent. His blood pressure was 180/100 mm of Hg. He had exaggerated tendon reflexes and extensor planter response on the left side. Other systemic examination revealed no abnormality.

Investigation revealed random blood sugar 10.2 mmol/L, serum creatinine 0.96 mg/dl, serum cholesterol 220 mg/dl, serum triglyceride 150 mg/dl, X-ray chest P/A view showed normal study, ECG showed features of left ventricular hypertrophy. C. T scanof brain revealed intracerebral haematoma with perifocal oedema (right) with intraventricular haemorrhage.

Patient was diagnosed as stroke with left sided hemiplegia caused by intracerebral haemorrhage with ventricular extension with hypertension and dyslipidaemia.

The patient was treated conservatively with general nursing care and physiotherapy.

Stroke due to haemorrhage is one of the commonest cause of acute confusional state and it is mostly due to hypertension. If the patient is managed conservatively, he may regain full consciousness although neurological deficits may persist. Control of known risk factors reduce the incidence of stroke in good number.


Mr. Abdul Latif, a 35 years old farmer, smoker, hailing from Chandpur was admitted on 6th August’08 with the complaints of low grade intermittent fever with evening rise of temperature associated with headache and repeated vomiting for 20 days, altered level of consciousness with disorientation for 1 day. He did not suffer from any major illness in the past. He had no recent history of travelling, no history of contact with a patient of tuberculosis.

On examination, the patient was drowsy and disoriented,GCS-11. His pulse -100/min. , BP – 100/70 mm Hg, temp- 100o F, respiratory rate-22/min. Signs of meningeal irritation-present. Planter response bilaterally equivocal.

Investigation revealed, Hb-11 gm%, total WBC count-11000 /cumm, with normal differential count. ESR-80 mm in first hour. X-ray chest revealed normal findings. Random blood sugar-4.0- mmol/L. Lumbar puncture revealed CSF pressure-high, color-straw. CSF study-protein 220 mg/dl, sugar 20mg/dl total WBC count-200 cells/cumm, differential count-lymphocyte 95%. Microbiology-no organism found.

Patient was diagnosed as Tubercular meningitis.

The patient was treated with general management and specific management by Anti-tubercular drugs with prednisolone. Patient regained full consciousness after 8 days and discharged after 10 days.

In our country, most of the people are in lower and lower middle class group. They cannot maintain proper nutrition, personal hygiene and moreover live in overcrowded area. So, infectious disease like tuberculosis in common. Prompt diagnosis, isolation, improvement of personal hygiene and treatment may prevent the incidence