Metabolic

Encephalopathy

dr. Yunus Tanggo Sp.PD. PhD

Department of Internal Medicine, Universitas Kristen Indonesia General
Hospital, Jakarta, Indonesia
 LEARNING OBJECTIVES
INTRODUCTION
COMMON METABOLIC
ENCEPHALOPATHIES
PATHOPHYSIOLOGY
CLINICAL SYMPTOM AND SIGN
DIAGNOSIS
MANAGEMENT
 INTRODUCTION
ENCEPHALOPATHY : Global cerebral
dysfunction
Metabolic encephalopathy brain
dysfunction due to metabolic disorder
Common Metabolic encephalopathies:
Hypertensive encephalopathy
Hepatic encephalopathy
Uremic encephalopathy
Encephalopathy with
Hypoglycemia/Hyperglycemia
 HYPERTENSIVE
ENCEPHALOPATHY
1% of patients with hypertension will
present with hypertensive crisis (end-
organ damage)
If hypertension remains untreated
mortality is >50% over next 12 months
Hypertensive encephalopathy is among
most serious presentations of uncontrolled
hypertension
May be due to acute crisis in setting of
medication noncompliance.
May be part of drug intoxication (cocaine,
 CLINICAL PRESENTATION
Present with headache, nausea, vomiting
and visual disturbance,
May present with seizures
Fundoscopic exam may show exudates,
hemorrhages, papilledema
Neuroimaging studies show subcortical
parietooccipital edema (PRES)

Fundus
 TREATMENT
Immediate treatment of hypertension is
the key
Reduce MAP by 25%
Use parenteral antihypertensive agents
and monitor BP in ICU setting with real
time arterial pressure monitoring
Calcium channel blockers or beta
blockers reduce BP without cerebral
vasodilatation
 HEPATIC
ENCEPHALOPATHY
Hallmark of advanced liver failure
CNS problems arise from accumulation of
toxins (ammonia, manganese, GABA,
various branched chain amino acids,
opioids) as well as cerebral edema
In cases were HE is due to alcohol abuse,
must remember other alcohol related CNS
problems such as Wernickes
encephalopathy, alcoholic cerebellar
degeneration, ICH, subdural hemorrhage.
 Diagnosis supported by history of
liver disease
Impaired cognitive function
Foul smelling breath (fetor hepaticus)
Asterixis
Elevated ammonia levels
Impaired consciousness
 STAGING HEPATIC
ENCEPHALOPATHY
Stage 1. mental slowness, anxiety,
impaired attention and calculation
Stage 2. Lethargy or apathy and
personality change
Stage 3. Worsening lethargy and
somnolence and confusion but still able to
respond to verbal stimuli
Stage 4. Hepatic coma which leads to
death if untreated (including
transplantation)
 TREATMENT
Late stage liver failure associated with
severe coagulopathy and failure of
gluconeogenesis
Correction of coagulopathy in setting of
active bleeding
Glucose infusions often necessary
Cerebral edema and coma are pre-terminal
events
Transplantation is ultimate therapeutic
intervention
 UREMIC
ENCEPHALOPATHY
Characterized by slowly progressive
dementia, psychiatric changes, speech
disorders, involuntary movements,
seizures,coma and death

May occur in acute or chronic renal failure

(AKI minimize secondary worsening)

Raised blood urea alone cannot be

responsible for the loss of consciousness but
the Metabolic acidosis, electrolyte
disturbances and Water intoxication due to
 TREATMEN
Treatment of uremic encephalopathy revolves
around management of the renal failure

Hemodialysis in setting of uremic symptoms

Remember to modify drug doses based on

estimated creatinine clearance of various drugs
 HYPOGLYCEMIA
Hypoglycemia is most commonly caused by drugs
used to treat diabetes mellitus or by exposure to
other drugs, including alcohol.

The lower limit of the fasting plasma glucose

concentration is normally approximately 70 mg/dL
(3.9 mmol/L), Glucose levels <55 mg/dL (3.0
mmol/L) with symptoms that are relieved promptly
after the glucose level is raised document
hypoglycemia.

Hypoglycemia can cause serious morbidity; if

severe and prolonged, it can be fatal. It should be
considered in any patient with episodes of
confusion, an altered level of consciousness, or a
CLINICAL PRESENTATION
Much more rapid onset.
Symptoms appear with blood sugars
of less than 2.5 mmol/l
Initially autonomic: sweating and
pallor, and then inattention and
irritability progressing to stupor,
coma, and frequent seizures.
Patients may be hypothermic.
MANAGEMENT
 Diabetic Ketoacidosis and Hyperosmolar
Hyperglycemic State

Hyperosmolar hyperglycemic state (HHS) and

diabetic ketoacidosis (DKA) represent two
distinct metabolic derangements manifested
by insulin deficiency and severe hyperglycemia

HHS occurs when insulin deficiency relative to

insulin requirements causes hyperglycemia,
which in turn leads to dehydration, ultimately
resulting in a severe hyperosmolar state.
 Essentials of Diagnosis :
Hyperglycemia > 600 mg/dl,
Serum osmolality > 320 mosm/kg,
No acidosis; blood pH above 7.3, serum
bicarbonate > 15 mEq/L, normal anion gap
(< 14 mEq/L)
Osmolality can be calculated using the formula
for effective osmolality (mOsm per kg)
normal values in humans are 280300 mosm/kg
 DKA occurs in the setting of more severe
insulin deficiency, when low circulating
levels of insulin lead not only to
hyperglycemia and dehydration but also to
the production of ketone bodies and acidosis

DKA is defined as the presence of all three

of the following: (1) hyperglycemia (glucose
>250 mg/dL), (2) ketosis, and (3) acidemia
(pH <7.3)
ETIOLOGY
PATHOPHYSIOLOGY
DIAGNOSTIC CRITERIAS
Thank You
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