A9. Unconsciousness due to metabolic origin Flashcards
Unconsciousness due to metabolic origin is usually a disorder of
disorder of awareness
Unconsciousness due to metabolic origin can manifest as
persistent vegetative state (PVS),
also called unresponsive wakefulness syndrome (from lecture).
General symptoms of Unconsciousness due to metabolic origin
- pupils are normal in size and reactive to light
- eye movements are usually full and conjugate
- depressed mental state
- confusion with impairment of consciousness
- depressed respiratory rate
- limb movements are symmetrically reduced and associated with hypotonicity.
- Hemiparesis can occur in:
*non-ketotic hyperosmolar coma, *hepatic encephalopathy.
*hyperglycemic encephalopathy.
*uremic encephalopathy.
Causes of Unconsciousness due to metabolic origin
● Deficiency of essential substrates (glucose, oxygen, vitamin B12)
● Exogenous toxins
(eg. drugs, heavy metals, solvents)
● Endogenous toxins/systemic metabolic diseases
(eg. uremia, hepatic encephalopathy, electrolyte imbalances, thyroid storm
Deficiency of essential substrates that can cause Unconsciousness due to metabolic origin
- glucose
- oxygen
- vitamin B12
Exogenous toxins that can cause Unconsciousness due to metabolic origin
- drugs,
- heavy metals,
- solvents)
example of Endogenous toxins/systemic metabolic diseases which cause Unconsciousness due to metabolic origin
- uremia,
- hepatic encephalopathy,
- electrolyte imbalances,
- thyroid storm
causes of Disorder of glucose metabolism (prolonged hypoglycemia)
Can be due to
* insulin overdose,
* fasting,
* alcohol intoxication and
* rarely insulinomas
how to differentiate between comatose state due to hypoglycemia
and a structural cause.
In hypoglycemia, pupillary light reactions may be intact, while in structural damage they
are usually absent
does hypoglycemia lead to focal necrosis in brain, brainstem or spinal cord?
Hypoglycemia does NOT cause focal necrosis in brain, brainstem or spinal cord.
They remain intact even in long-standing, severe hypoglycemia
In Disorder of glucose metabolism (prolonged hypoglycemia) what is damaged
The superficial layers of the cortex are damaged,
but laminar necrosis (as in global ischemia) is NOT seen
Disorder of glucose metabolism (prolonged hypoglycemia - where does necrosis occur
Necrosis also develops in the
* superficial layers of the cortex
* hippocampus,
* caudate nucleus and
* granular cells of dentate gyrus
what blood glucose level can cause coma?
Blood glucose levels <0,6 mmol/l can cause coma
Hyperosmolar hyperglycemia results from
hyperosmolar effect of severe hyperglycemia
Hyperosmolar hyperglycemia can cause patient to have
involuntary movements,
seizures and
hemiparesis
is vascular thrombosis common in Hyperosmolar hyperglycemia
not uncommon
does ketoacidosis occur in Hyperosmolar hyperglycemia
Ketoacidosis is mild or does not occur
Diabetic ketoacidosis occurs in patient with
known diabetes, but can also be the first manifestation
Diabetic ketoacidosis is often precipitated by
infection
or
poor medical compliance
Diabetic ketoacidosis - what metabolites are accumulated
accumulation of acetone and ketone bodies
patients with Diabetic ketoacidosis present with
- progressive neurological impairment
- with lethargy, and
- ultimately coma
Symptoms of diabetic ketoacidosis
- dehydration (due to osmotic diuresis),
- fatigue,
- weakness,
- headache,
- abdominal pain,
- Kussmal breathing,
- confusion,
- coma
causes of Hypoxia
- May also occur at high altitudes (low O 2 tension of the atmosphere and in drowning
○ Reduced arterial oxygen pressure: e.g. lung disease or PE
■ Hypoxia due to PE causes confusion and lethargy before loss of consciousness
○ Reduced hemoglobin to carry oxygen: anemia or blood loss
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■ pO 2 does not drop, but substrate availability is decreased or O 2 fails to bind to
hemoglobin
○ Reduced flow of blood containing O 2 (ischemic hypoxia): due to reduced cardiac output
→ reduced cerebral blood flow
○ Biochemical block of cerebral utilization of O 2 : e.g. cyanide poisoning (rare), also called
histotoxic hypoxia
causes of Reduced arterial oxygen pressure:
- lung disease
- or PE
■ Hypoxia due to PE causes confusion and lethargy before loss of consciousness
causes of Reduced hemoglobin to carry oxygen:
- anemia or
- blood loss
■ pO2 does NOT drop, but substrate availability is decreased or O2 fails to bind to hemoglobin
cause of Reduced flow of blood containing O 2 (ischemic hypoxia):
due to reduced cardiac output
→ reduced cerebral blood flow
causes of Biochemical block of cerebral utilization of O 2
- cyanide poisoning (rare), also called
histotoxic hypoxia
Hypoxia due to PE causes confusion and lethargy before what?
loss of consciousness
if pO 2 drops under 40 mmHg
Consciousness is lost in some seconds
how long can Hypoxic hypoxia (without ischemia) be tolerated without permanent damage
can be tolerated for 10-40 minutes without permanent damage to the brain,
even if pO 2 is below 20 mmHg
CO intoxication leads to
bilateral necrosis of globus pallidus
is grey matter or white more vulnerable to hypoxia
list structure most vulnerable
grey matter is more vulnerable than white
Vulnerability to hypoxia (most to least),
○ Frontal cortex (most)
○ Hippocampus, parietal/occipital cortex
○ Basal ganglia/cerebellum
○ Brain stem
Symptoms of hypoxia - pupil and eye
Pupils: large-reactive
Eye movements: no movement – conjugate (if severe)
Hypercapnia symptoms
- headache,
- confusion,
- disorientation,
- involuntary movements,
- papilledema,
- depressed limb reflexes,
- extensor plantar response
if PCO2 > 50 mmhg in
COPD
or
obesity-ventilation syndrome
CO2 narcosis may occur
when does co2 narcosis occur in COPD or obesity-ventilation syndrome?
if pco2 over 50 mmhg
Hypothermia
Common in
- alcoholics with Wernicke encephalopathy (deficiency of B1)
Renal/uremic encephalopathy is a sign of
acute renal failure
what happens in Renal/uremic encephalopathy
- Brain amino acid metabolism is also impaired, and
- causes an imbalance between excitatory and inhibitory neurotransmitters
or - accumulation of false neurotransmitters
Renal/uremic encephalopathy EEG shows
Slow waves are found on the EEG
can Renal/uremic encephalopathy be reversed?
condition is reversed with dialysis,
but may take 1-2 days before it is totally reversed
Hepatic encephalopathy onset can be
Can have acute or chronic onset
causes of hepatic encephalopathy
- increased ammonia,
- false neurotransmitters,
- endogenous benzodiazepine-like structures,
- abnormal fatty acid metabolism,
- free radical damage,
- cerebral edema and
- increased mercaptans
Symptoms of
Hepatic encephalopathy
○ Pupils: small-reactive
○ Eye movements: no movement – dysconjugate (if severe)
○ Increased respiratory rate
○ Asterixis, myoclonus, dysarthria, ataxia, hyperreflexia, hemiparesis
how does patient with hepatic encephalopathy appear in early phase vs late
- At earlier phases the patient is in an
agitated confusional state - Unconsciousness and coma are the most severe stages.
Hepatic encephalopathy- Neurological signs in comatose patients include
- hemiparesis,
- ocular bobbing,
- dysconjugate eye movements and
- tonic downward deviation of the eyes
In deep coma what can be present
hepatic encephalopathy
- decerebrate posture and
- agonal respiration can be present
Hepatic encephalopathy EEG shows
The EEG is always abnormal (shows triphasic slow waves)
Electrolyte disturbances
● Hypernatremia
● Hyponatremia
● Hypercalcemia,
● hypocalcemia,
● hyperkalemia
● hypokalemia
● hypomagnesemia,
Hypernatremia present as
Hyperosmolar diabetic hypernatremia:
mostly in elderly diabetic patients
what does hypernatremia cause to the brain
○ Leads to osmotic dehydration of the brain
Hyponatremia
range
Na <126 mmol/l
Hyponatremia causes
- primary renal disease,
- osmotic diuresis,
- adrenal insufficiency,
- vomiting,
- diarrhea,
- burns,
- ascites,
- peritonitis,
- edema,
- dilution,
- sickle cell syndrome,
- hyperglycemia,
- SIADH
Hyponatremia treatment
slow correction of the sodium, over several days
○ Too fast correction can cause central pontine myelinolysis (symptoms can be vertical
gaze palsy, tetraplegia)
○ Too fast correction of hyponatremia can cause
central pontine myelinolysis (symptoms can be:
vertical gaze palsy,
tetraplegia)
central pontine myelinolysis symptoms
- vertical gaze palsy,
- tetraplegia)
which electrolyte disturbances Can cause coma in severe cases
- Hypercalcemia,
- hypocalcemia,
- hypomagnesemia,
- hypokalemia,
- hyperkalemia
- hypernatremia
- hyponatremia
Other causes of Unconsciousness due to metabolic origin
● Hypothyroidism
● Lactic acidosis
● Addison’s disease
