Confusion

Approach to metabolic causes

By
Fatma Hamdy Fouad
Lecturer of Internal medicine.
Mansoura University
Female patient aged 65 years DM & HTN 10 years ago, presented to
the ER with confusion 1week

What is confusion?

What is the cause?

How can we reach the diagnosis?

Consciousness:
• Ill defined & poorly understood term.
• Confusion occur if either (RAS, cerebral cortex or
thalamus ) malfunction.
• Minor defects may be subtle and difficult to be detected.
• Consider the possibility of multifactorial causes.
 .Normal consciousness

Intact
Cerebral
reticular
cortex &
activating
thalamus
system (RAS)

.Arousal .Cognition
Definitions:
.Definition .Term
.Global impairment of mental function .Confusion
Abrupt decline in cognitive function. Delirium
Follow fluctuating course.
Accompanied by impaired attention.
Associated features: (inverted sleep rhythm, delusion,
hallucinations).
Chronic progressive decline in cognitive function without .Dementia
disturbance in consciousness
Unresponsiveness but aroused .Stupor
State of decreased awareness and alertness (patient may appear .Lethargy
wakeful)
A sleep-like state, not arousable to consciousness (GCS<9) .Coma
 What are causes of confusion?
Drugs/ Organ
Metabolic. CNS causes failure
toxins

• Trauma: intracranial
hemorrhage. • Hepatic
• Hypoglycemia. • Alcohol. • Infection: meningitis or encephalopathy.
• Hyperglycemic • Opioids. encephalitis. • Uremic
comas • TCA. • Stroke.
encephalopathy.
• Major electrolyte • Barbiturates. • Subarachnoid
hemorrhage. • Respiratory
disturbance. • Recreational
• Tumor. failure.
• Hypothyroidism. drugs. • Hypertensive • Shock.
• Metabolic acidosis. • CO encephalopathy.
• Psychogenic.
How can we reach the diagnosis?
Initial emergency
evaluation

Neurological evaluation

Search for
metabolic cause

Drugs / toxins or
others
1 Initial emergency evaluation:
1 Initial emergency evaluation:
Ensure patent airway.

Pulse oximeter & ABG  treat hypoxia

or hypercapnia urgently.

Shock  assess & treat

Assess conscious level.

Glasgow coma scale:

• Used to record conscious

level.
• Less than 15 altered
consciousness.
• Less than 8  coma.
1 Initial emergency
evaluation: blood glucose &
vital signs.
• Blood glucose < 55mg/dl  treat with IV
dextrose or glucagon.
• Hypothermia  Assess & rewarm (suspect
myxedema coma).
Hypoglycemia:

• Whipple triad.
Hypoglycemia:
Clinical features:
• Typically occur first.
Adrenergic • Caused by autonomic nervous system activity.
:symptoms • Palpitations, sweating, anxiety, tremor, tachycardia.

Neuroglycopenic • Caused by decreased activity of CNS.

• Dizziness, headache, clouding of vision, mental
:symptoms dullness, fatigue, confusion, seizures, coma.
Hypoglycemia:
History & examination:
• Last meal.
• Known diabetes.
• Prior similar episodes.
• Drug therapy and compliance.
• Liver/renal/endocrine/neoplastic disease
• Alcohol or drug use
Hypoglycemia:
Treatment:
• IV access and rapid blood glucose measurement
• D50W 50 mL IV push.
• Glucose PO if mental status permits if IV access not possible.
• Glucagon 1-2 mg IM.
• Frequent BG monitoring.
• Full meal as soon as mental status permits ƒ
• If episode due to long acting insulin, or sulfonylureas, watch for
prolonged hypoglycemia.
• Search for cause.
2 Neurological evaluation:
• Meningeal irritation signs.
.CNS infection • Fever.
• Maculopapular rash.

Intracranial • GCS<8.
• Signs of lateralization.
.pathology • Head trauma

Witnessed • Post ictal state.

seizures
3 Search for metabolic cause/
organ failure:
Organ
Metabolic. failure

• Hypoglycemia. • Hepatic encephalopathy.

• Hyperglycemic comas. • Uremic encephalopathy.
• Major electrolyte • Respiratory failure.
disturbances (Na, K, Ca, PO4, • Shock.
Mg)
• Thyroid disorders.
• Metabolic acidosis.
History:
.Definition .Term
.Acute onset  CNS hemorrhage, ischemia or cardiac cause Onset & course
Gradual onset progressive course  toxic, metabolic or progressive CNS
.cause
Baseline conscious level. Preceding events
Seizures (post ictal state).
Fever (infection)
.DM  hypoglycemic or hyperglycemic comas .Past medical history
.Liver cell failure  hepatic encephalopathy
.CKD  uremic encephalopathy, electrolyte disturbances
.Previous strokes  recurrent stroke
.Opioid Drug history
.Barbiturates
.Recreational drugs
)Diuretics  electrolyte disturbance
.Oral antidiabetic drugs  hypoglycemia
Examination:
.Definition .Term
.ABP  shock or hypertensive encephalopathy Vital signs
Pulse  AF (risk factor for stroke)
.tachycardia or bradycardia (arrhythmia)
RR  tachypnea (metabolic acidosis, DKA, chest infection)
Temperature  fever (infection)
hypothermia (myxedema coma)
Dehydration. .General examination
Stigmata of chronic liver disease.
Malnutrition.
.Signs of lateralization Neurological
.Meningeal irritation signs examination
.Crepitations Pneumonia Chest examination
.Ascites, splenomegaly, shrunken liver  hepatic encephalopathy Abdominal
.Distension  constipation .examination
.Rigid tender abdomen  acute abdomen
Investigations:
.Definition .Term
.Hypoglycemia .Blood glucose
.Hyperglycemia (DKA,HHS)
.Leukocytosis  infection CBC
Anemia & thrombocytopenia  TMA
Hypoxia & hypercapnia  CO2 narcosis. ABG
Metabolic acidosis  DKA
Uremic encephalopathy .Serum creatinine
Na, Ca, Mg, K & po4 .Electrolytes
.Fulminant hepatic failure Liver function tests &
INR
.Acute MI may manifest as syncope (elderly) ECG
.Arrhythmia
.CT brain, chest X ray, abdominal US .Radiology
Major metabolic derangements:

Hyperglycemic Electrolyte Hepatic

comas disturbances encephalopathy

Thyroid storm &

Uremic
myxedema
.encephalopathy
coma
Major metabolic derangements:

Hyperglycemic Electrolyte Hepatic

comas disturbances encephalopathy

Thyroid storm &

Uremic
myxedema
.encephalopathy
coma
Major metabolic derangements:

Hyperglycemic Electrolyte Hepatic

comas disturbances encephalopathy

Thyroid storm &

Uremic
myxedema
.encephalopathy
coma
DKA:

Type 1 DM
DKA:
 Investigations:

• Ketonemia. • High anion gap

• High blood glucose
• Urine +ve for ketone metabolic acidosis.
• Urine +ve for glucose.
bodies. • Low HCO3

Electrolyte
disturbance (K& Na)
DKA: K replacement
Treatment:
• The main treatment.
• Normal saline.
Rehydration • D5W if BG below 250mg/dl

• Critical for acidosis to resolve.

Insulin. • Use only regular insulin.
• Check blood glucose hourly.

HCO3
• Life threatening acidosis.
HHS:
Pathophysiology:

Type 2 DM

Precipitating
factor (stroke or
AMI).

Small amount of
insulin prevent
ketosis.
HHS:
Investigations:

.Blood glucose • Markedly elevated 600mg/dl or greater.

Na & • Mild dehydration  hyponatremia (effect of hyperglycemia).

• Severe dehydration hypernatremia.
.osmolarity • Increased osmolarity.

• PH>7.3.
ABG • No acidosis or ketosis.
HHS: K replacement
Treatment:
• The main treatment.
• Normal saline.
Rehydration • D5W if BG below 250mg/dl

• Lower dose than DKA.

Insulin. • Use only regular insulin.
• Check blood glucose hourly.
Major metabolic derangements:

Hyperglycemic Electrolyte Hepatic

comas disturbances encephalopathy

Thyroid storm &

Uremic
myxedema
.encephalopathy
coma
 • Spectrum of potentially reversible
neuropsychiatric syndromes secondary to
liver disease.
Hepatic
• Portosystemic shunt around hepatocytes
encephalopathy: and decreased hepatocellular function
Definition & increase level of systemic toxins (believed to
pathophysiology: be ammonia from gut, mercaptans, fatty
acids, amino acids) which go to the brain.
• Diagnosis of exclusion.
 Nitrogen load (GI bleed, protein load from
food intake, renal failure, constipation).

Drugs (narcotics, CNS depressants).

Hepatic
encephalopathy: Electrolyte disturbance (hypokalemia,
alkalosis, hypoxia, hypovolemia).
Precipitating
factors: Infection (spontaneous bacterial
peritonitis).

Deterioration in hepatic function or

superimposed liver disease
 Treat underlying precipitating factors.

Decrease generation of nitrogenous

compounds  decrease dietary protein
Hepatic
Lactulose: titrated to achieve 2 to 3 soft
encephalopathy: stools per day.
Treatment:
Antibiotics (metronidazole, rifaximin).

Lactulose enemas
Major metabolic derangements:

Hyperglycemic Electrolyte Hepatic

comas disturbances encephalopathy

Thyroid storm &

Uremic
myxedema
.encephalopathy
coma
 • Organic brain disorder.
• Develop in patients with AKI or CKD.
• When e GFR remains below
Uremic 15ml/min.
encephalopathy: • Manifestations may be:
- Mild symptoms: lassitude & fatigue.
- Severe symptoms: coma & seizures.
• Symptoms are reversible with dialysis.
6 Drug or alcohol toxicity:
7 Further investigations
• Toxicology screen.
• Hypertensive encephalopathy.
• EEG  unresponsive state.
• MRI brain.
• Psychogenic unresponsiveness.
Wernicke encephalopathy:
• Neurological disorder induced by acute thiamin (vitamin B1) deficiency.
• Associated with:
- Chronic alcoholism. - Prolonged starvation.
- Hyperemesis gravidarum. - Bariatric surgery.
• Manifest as triad of:
- Confusion.
- Cerebellar dysfunction (ataxia).
- Ophthalmoplegia.
• Korsakoff amnesia:
- Memory loss & confabulation.
• Mainly clinical diagnosis.
• Treatment by parenteral thiamin.