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Metabolic Encephalopathy

Brain Disease Metabolic

Metabolic encephalopathy is a transient or permanent impairment of brain function resulting from physiological insufficiency or aberrant metabolic processes accompanying certain systemic illness such as diabetes or liver disease. Timely recognition and treatment of the predisposing condition can reverse the potential damage to the brain.


Presentation

Metabolic encephalopathies generally present as impairment of brain function, including loss of consciousness. The latter is presumed to be due to failure of the neocortex [6], to coordinate with other forebrain structures involved in cognition to stimulate the ascending reticular activating system (ARAS). Ascend from the ARAS via thalamic synaptic relays to the neocortex is mediated by specific brainstem nuclei and associated fibers. Thus, metabolic encephalopathies result from biochemical aberrations at both neocortex and ARAS centers. Initially, respiration rate decreases and the pupils are small but reactive. Asterixis, also termed “flapping tremor” observed in sedative intoxication, uremia and hepatic disease. Asterixis is caused by the loss in voluntary muscle postural tone of the head, tongue, limbs or trunk. In advanced stages seizures occur as in acute liver failure and hypoglycemia. Concomitant loss of brainstem respiratory control result in Cheyne-Stokes breathing. Lack of  movement control and coordination due to focal metabolic changes in basal ganglia and the cerebellum are seen in metabolic encephalopathies such as those associated with avitaminosis and ingestion of toxic substances.

The symptoms of metabolic encephalopathy are:

Early recognition of these manifestations and immediate treatment may serve to reverse the encephalopathy, prevent death or at least diminish the subsequent damage to the brain.

Myxedema
  • Hypotension, unresponsive to volume expansion, points to intoxication with barbiturates or opiates, myxedema, or Addisonian crisis. In this setting, occult sepsis must always be ruled out before treating for specific metabolic derangements.[aneskey.com]
Cheyne-Stokes Respiration
  • ICD 10 … Wikipedia Glycine encephalopathy — (Non ketotic Hyperglycinemia) Classification and external resources Glycine OMIM 605899 … Wikipedia Cheyne-Stokes respiration — ICD 10 R06.3 ICD 9 786.04 MeSH D002639 … Wikipedia delirium — Also known as acute[hallucinations.enacademic.com]
  • Cheyne-Stokes respiration, a rhythmic cycle of waxing and waning hyperpnea/apnea, is another pattern that is occasionally seen in metabolic encephalopathy caused by uremia or hypoxia, but more commonly this indicates bilateral structural lesions of the[aneskey.com]
  • […] neurological signs may include involuntary grasping and sucking motions, nystagmus (rapid, involuntary eye movement), jactitation (restless picking at things characteristic of severe infection), [ citation needed ] and respiratory abnormalities such as Cheyne-Stokes[en.wikipedia.org]
  • Other serious symptoms that may occur include: lethargy, dementia, seizures, tremors, muscle twitching and myalgia, Cheyne-Stokes respirations (an altered breathing pattern seen with brain damage and coma), and coma.[medicinenet.com]
Asterixis
  • Asterixis, also termed “flapping tremor” observed in sedative intoxication, uremia and hepatic disease. Asterixis is caused by the loss in voluntary muscle postural tone of the head, tongue, limbs or trunk.[symptoma.com]
  • Subacute uremia and pulmonary failure produce asterixis accompanied by myoclonus, which presents a picture of almost constant muscular jerking movements.[aneskey.com]
  • . • Motor findings that are strongly suggestive of a metabolic or toxic encephalopathy include postural-action tremor, asterixis, and multifocal myoclonus. • In comatose patients with metabolic or diffuse or bihemispheric disturbances in cerebral function[medlink.com]
  • Asterixis cannot be elicited in patients with hepatic encephalopathy in what stage? A. 1 B. 2 C. 3 D. 4 E. 5 D. Stage 4 The patient is already comatose so you cannot do the test. There is no stage 5.[brainscape.com]
Hypertension
  • Case Presentation: A 52-year-old African American male with a history of Diabetes Mellitus Type 2, Hypertension, and Hyperlipidemia presented to the Emergency Department with complaints of dizziness and fluctuating level of consciousness.[shmabstracts.com]
  • The basal metabolic rate (BMR) is the rate of energy consumption by the body when it is completely at rest. metabolic syndrome characterized by hypertension, insulin resistance, an abnormal plasma lipid profile, and obesity. metabolic toxins include histamine[medical-dictionary.thefreedictionary.com]
  • […] of CNS symptoms after the metabolic problem is corrected Encephalopathy causes include: VIITTAMIN: Vascular, Inlammatory, Infectious, Traumatic, Toxins, Autoimmune, Metabolic, Idopathic/Genetic; Neoplastic A major vascular cause of encephalopathy is: Hypertensive[quizlet.com]
  • This condition is linked to hypo/hypertension; hyperviscosity syndrome; cardiovascular disease (including cardiac arrest); microvascular diseases; •Stokes-Adams syndrome, cardiac arrhythmias; and hypersensitive carotid sinus.[symptoma.com]
  • Hypertensive Encephalopathy Indexed in ICD-10-CM to I67.4 is caused by extreme high blood pressure levels. Most often the effects are reversible. Treatment is geared towards decreasing blood pressure.[hiacode.com]
Alopecia
  • Clinical findings include seizures, ataxia, alopecia and dermatitis with atypical findings of myoclonic jerks, neuropathy and spastic paraparesis.[ncbi.nlm.nih.gov]
Seizure
  • […] are necessary to control seizures and prevent permanent brain damage.[epilepsy.com]
  • In advanced stages seizures occur as in acute liver failure and hypoglycemia. Concomitant loss of brainstem respiratory control result in Cheyne-Stokes breathing.[symptoma.com]
  • Symptoms and signs usually suggest a generalized disturbance of brain function: alterations in the level of consciousness; diffuse and, occasionally, focal motor abnormalities; and seizures.[ncbi.nlm.nih.gov]
  • Clinical findings include seizures, ataxia, alopecia and dermatitis with atypical findings of myoclonic jerks, neuropathy and spastic paraparesis.[ncbi.nlm.nih.gov]
  • Need WIDE variations to change neuronal and glial dysfunction Because the brain is location-based, global disruption of metabolic homeostasis can result in: Behavior change, poor coordination, ataxia, confusion, seizures, stupor and coma; May be a lag[quizlet.com]
Confusion
  • Encephalopathy causes confusion, abnormal thought processes, poor memory, hallucinations, and psychotic thinking.[healthcare-online.org]
  • Alcohol intoxication can cause __ in the nervous system Euphoria, ataxia, confusion, coma, death Alcohol withdrawal can cause __ in the nervous system Delirium tremens (Tremor, hallucinations, confusion, autonomic features); Seizures within 48 hours Wernicke's[quizlet.com]
  • The symptoms of metabolic encephalopathy are: Lapse of memory Confusion or agitation Habitual sleeplessness Difficulty in speaking Changes in behavior and personality Mental confusion Tremor Muscle stiffness Stupor or coma Uncontrollable movements, or[symptoma.com]
  • There can be neurological changes such as difficulty with memory, tremors, involuntary twitching, seizures, disorientation and mental confusion.[tandurust.com]
  • Symptoms include, confusion, disorientation, hallucinations, memory loss , abnormal eye movements including nystagmus and double vision , incoordination and imbalance.[healthtap.com]
Stupor
  • The symptoms of metabolic encephalopathy are: Lapse of memory Confusion or agitation Habitual sleeplessness Difficulty in speaking Changes in behavior and personality Mental confusion Tremor Muscle stiffness Stupor or coma Uncontrollable movements, or[symptoma.com]
  • The symptoms of metabolic encephalopathy include as: Agitation and confusion Forgetfulness Insomnia Change in behavior Stupor or coma Stiffness of muscles Tremor in finger and hands. Uncontrolled movement of hands and legs. Seizures in rare cases.[tandurust.com]
  • The next day patient was found stuporous and only awakened by deep stimuli. Pupils were anisocoric, non-reactive and vertical gaze palsy was noted. CT scan of head without contrast did not show any bleed.[shmabstracts.com]
  • Forgetfulness Disorientation Insomnia ]] Muscle stiffness or rigidity ]] Tremor ]] (particularly a flapping tremor of the hands) Difficulty speaking Asterixis (rapid momentary loss of tone in the muscles) Uncontrollable movements or ]] seizures ]] (rare) Stupor[empowher.com]
Agitation
  • Patient treated with IV Haldol 5mg PRN for agitation, IV Levofloxacin, moved closer to nurses station for observation due to agitation and confusion. Query: Encephalopathy has been documented within the medical record.[cdiarchive.com]
  • Metabolic encephalopathy is, thus, a syndrome of global cerebral dysfunction induced by systemic stress, and can vary in clinical presentation from mild executive dysfunction or agitated delirium, to deep coma with decerebrate posturing.[medlink.com]
  • Level of alterness, orientation, and attention The hallmark of encephalopathy is: Impaired ATTENTION (early finding in delirium, late finding in dementia) Symptoms of encephalopathy include: Hallucinations, delusions, agitation or lethargy; Irritation[quizlet.com]
  • The condition is most commonly seen in older individuals There are 3 types of Delirium: Hyperactive Delirium, which is characterized by restlessness, agitation, rapid mood changes, and hallucinations Hypoactive Delirium, which is characterized by inactivity[dovemed.com]
  • The symptoms of metabolic encephalopathy are: Lapse of memory Confusion or agitation Habitual sleeplessness Difficulty in speaking Changes in behavior and personality Mental confusion Tremor Muscle stiffness Stupor or coma Uncontrollable movements, or[symptoma.com]
Tremor
  • Symptoms Symptoms of metabolic encephalopthy include: Confusion or agitation Disorientation Insomnia Forgetfulness Tremor (flapping tremor of the hands) Difficulty in speaking Behavioral change Asterixis (rapid momentary loss of tone in the muscles) Muscle[symptoma.com]
  • There can be neurological changes such as difficulty with memory, tremors, involuntary twitching, seizures, disorientation and mental confusion.[tandurust.com]
  • ]] (particularly a flapping tremor of the hands) Difficulty speaking Asterixis (rapid momentary loss of tone in the muscles) Uncontrollable movements or ]] seizures ]] (rare) Stupor or ]] coma ]] These problems can develop quickly.[empowher.com]
  • […] encephalopathy is: Impaired ATTENTION (early finding in delirium, late finding in dementia) Symptoms of encephalopathy include: Hallucinations, delusions, agitation or lethargy; Irritation to light touch; Withdraw limbs unequally; Asterixis, myoclonus, tremor[quizlet.com]
  • Tremors are rhythmic, involuntary oscillatory movements seen in all limbs and often exaggerated during voluntary movement.[aneskey.com]

Workup

Metabolic Encephalopathy is one of many conditions manifested by aberrant brain function, with diverse etiology ranging from infection, structural damage, systemic diseases, and poisoning. Differential diagnosis entails recognition of this multifarious causes and the importance of prompt intervention to minimize or prevent permanent damage to the brain. Acute encephalopathy in a child may be due instead to sepsismeningitis or structural abnormalities as in intracranial hemorrhage or brain tumor. One should be aware of the possibility of shaken baby syndrome. Inborn errors of metabolism should be ruled out in neonates.

Laboratory studies

  • Routine blood tests: CBC; coagulation; electrolytes; calcium, magnesium, phosphate, glucose, creatinine; BUN, liver function tests, bilirubin, ammonia, and arterial blood gases [7].
  • Blood and CSF cultures for infection.
  • Toxicologic screening of blood and urine for poisoning.
  • Thyroid function tests and serum cortisol. concentrations for endocrinopathy [8] [9].

On the basis of clinical findings, blood and urine test should be done for inborn errors of metabolism.

Incase of new born patients metabolic screening studies result should re-examine and repeated if necessary.

Imaging studies

  • CT scan and MRI to exclude structural encephalopathy or trauma.
  • Cranial ultrasonography for newborns, with x-ray skeletal survey for shaken baby syndrome.

Electroencephalography

EEG can serve to confirm global brain dysfunction and to exclude subclinical seizures and epilepsy with higher sensitivity.

Slowing
  • Slow activity that is prominent frontally, with deep triphasic waves (in the 2- to 4-Hz range), is characteristic of hepatic encephalopathy but can be seen in renal failure too [ 6 ].[aneskey.com]
  • They can also be registered in patients with septic encephalopathy together with diffuse slow theta/delta activity [Figure 1]. [40] Figure 1: Electroencephalogram in a patient with septic encephalopathy – slow theta delta activity Click here to view Use[neurologyindia.com]
  • The realization was slow in coming that the same injury to the brain could occur in football players, and that the most popular sport in the country could be a potential cause of psychiatric disturbances and early dementia.[medicinenet.com]
  • Your doctor may recommend nutritional supplements to slow the damage to your brain, or a special diet to treat underlying causes. In some cases of the disease, such as when the brain does not receive enough oxygen, you may slip into a coma.[healthline.com]
Triphasic Waves
  • Slow activity that is prominent frontally, with deep triphasic waves (in the 2- to 4-Hz range), is characteristic of hepatic encephalopathy but can be seen in renal failure too [ 6 ].[aneskey.com]
  • Furthermore, in these cases, other epileptic patterns in the form of spikes or sharp waves can also be detected. [39] However, triphasic waves are not specific only for hepatic encephalopathy.[neurologyindia.com]
Generalized Slowing
  • In the cases of encephalopathy, EEG can register generalized slowing or suppression of the EEG reactivity, loss of fast rhythm with occurrence of diffuse slow activity (theta and delta), presence of particular EEG patterns (focal or generalized), intermittent[neurologyindia.com]

Treatment

Delirium should be treated as a medical emergency. Monitoring of respiratory and circulatory functions is first priority, with neurological, laboratory and neuroimaging evaluations. Early recognition of the predisposing factor is essential. The patient should be allowed to recuperate in a placid, stress-free environment and encouraged to engage in cognitive activities.

Analgesic may be given for pain control. Antipsychotics, such as haloperidol in low, frequent doses (1-5 mg IV q 4-6 hours) with monitoring of the electrocardiographic QTc interval and normal magnesium levels, quetiapine (25-100 mg/day po) or olanzapine (2.5-7.5 mg/day po) have been used although without FDA approval. Recent studies suggest increased mortality with this treatment in the elderly [10]. Other deleterious effects of these drugs are extrapyramidal movement disorders and neuroleptic malignant syndrome. Benzodiazepines are used in cases of alcoholism and cocaine withdrawal. Trials with dexmedetomidine versus midazolam or lorazepam decreased the occurrence and shortened the episodes of delirium [11].

Prognosis

Prognosis of encephalopathy open link depends on the underlying cause and the potential for reversing or eliminating this cause. Thus, recovery varies among patients and poor prognosis could lead to complete loss of brain function or death. Prompt diagnosis and intervention is important as exemplified in the management of hypoglycemic patients. Patients given glucose at the onset of symptoms recover completely. Delayed treatment may lead to seizures or coma which may be reversed within hours or days with partial recovery. However, long or multiple delays can be fatal.

Etiology

The causes of metabolic encephalopathies are diverse ranging from pathophysiologic states, peripheral organ dysfunctions, infection, systemic diseases and poisoning. The most common toxic agent is alcohol [1].

Major causes of metabolic encephalopathies:

Hypoxia occurs when the brain is deprived of oxygen. In anemia, red blood cells are not able to deliver sufficient oxygen to the brain. In pulmonary disease and alveolar hypoventilation diminished blood flow likewise compromise the oxygen requirement for normal brain function.

Ischemia is the result of narrowing of small blood vessels, thus, decreasing blood flow in the brain. This condition is linked to hypo/hypertension; hyperviscosity syndrome; cardiovascular disease (including cardiac arrest); microvascular diseases; •Stokes-Adams syndrome, cardiac arrhythmias; and hypersensitive carotid sinus.

Systemic diseases are subject to derangement of their normal functions and the body's metabolic processes, thus, predisposing to oxygen deficit in the brain. These disease are: acid-base, electrolytes and fluid imbalances; vitamin deficiency; hepatic disease; renal failure; paraneoplastic syndromes; pancreatic disease; endocrine dysfunction (hypo/hyperglycemia, hyperosmolarity); vasculitis; infections; and sepsis.

Toxic agents poison brain tissues and cells in various ways, even taken unintentionally, like drugs and alcohol, or accidentally like insecticides. These are: alcohol; sedatives; narcotics; antibiotics and other drugs for chemotherapeutic purposes; psychiatric medications; heavy metals; and solvents.

Toxic metabolic encephalopathy can also include medication drug ingestions side effects or affecting the chemical transmitters in the brain called neurotransmitters; dopamine, serotonin, acetylcholine, GABA and glutamine help nerve endings pass electrical signals between brain cells. Alterations in these transmitters can decrease brain function. Concentrations of neurotransmitters and abnormal function can be seen in seizure disorders and Alzheimer's disease.

Epidemiology

The diverse nature of metabolic encephalopathy makes it difficult to obtain population-based studies for epidemiological assessment. One study report that patients with an eGFR of less than 10 mL/min manifested some degree of encephalopathy although the patients were not clearly symptomatic. In one pediatric study, 40% of the children with a BUN level greater than 90 mg/dL were considered positive for encephalopathy. These children were more likely to develop convulsions as BUN levels increased [2].

Sex distribution
Age distribution

Pathophysiology

Research aims to understand brain function and the underlying mechanisms that cause metabolic encephalopathies. As in other encephalopathies loss of brain function is basically attributed to a disturbance of blood brain barrier and changes in the amino acid and neurotransmitter conduits. Researchers have identified vascular factors, infection  and endotoxins in the pathophysiology of the disorder[3]. Histopathologic findings in hepatic and vascular encephalopathies include tissue edema, hypoxia, and necrosis. Astrocytes have been found to undergo hyperplasia and morphologic changes resembling Alzheimer type II cells [4] [5].

Prevention

To help avoid the risk of coma:

  • Seatbelt should be worn at all times when driving, to prevent traumatic head injury. Infants and small children should be safely installed in a child safety seat.
  • Passengers 12 years and younger should be in the back seat of a vehicle.
  • Helmet should be worn while biking, rollerblading, playing contact sports, riding a motorcycle, and similar activities in which head injury is imminent.
  • Athletic mouth guards are required while engaged in sports.
  • Abstain from alcohol or drugs when driving.
  • Diabetics should consult their doctors for regular monitoring of blood sugar levels.
  • When ill or on prescribed medication, consult a doctor or health care provider for advise and appropriate precautionary measure.
  • Avoid overdosing. Avoid being exposed to poisons or toxins.

Summary

Metabolic encephalopathy is an impairment of brain function resulting from the pathophysiological processes which occur in peripheral organ dysfunction such as diabetes, cardiovascular disorder, liver disease, and renal failure. The damage to the brain may be transient or permanent and reversible if the predisposing condition is treated or eliminated. Timely medical intervention is essential to prevent secondary structural abnormalities in the brain.

The two major types of metabolic encephalopathy are:

  1. Physiologic: Glucose, oxygen or metabolic cofactors (which are usually vitamin-derived) deficits, manifested by hypoxia, hypoglycemia, ischemia, hypercapnia and avitaminosis.
  2. Pathologic, as a result of other systemic disorders: hepatic encephalopathy, uremic and dialysis encephalopathies.

Encephalopathy due to abnormalities in brain chemistry and coma can occur. A variety of concomitant conditions such as vitamin deficiencies, hereditary disease, neuroendocrine disorders may cause brain dysfunction. Toxic encephalopathy can be traced to exposure to heavy metals and organic solvents. Ethanol can damage the brain permanently in the presence of avitaminosis and protein-calorie malnutrition. Hepatic encephalopathy has been linked to brain damage secondary to alcoholic cirrhosis.

Patient Information

Metabolic encephalopathy is a temporary loss of brain function which may develop in intensive care unit patients being treated for some other systemic disease. As such, it serves to predict deterioration of the patient's condition or progression of organ dysfunction that could lead to hypoxia or accumulation of toxins in the bloodstream. Early recognition and prompt medical intervention could reverse the condition or at least prevent permanent damage to the brain. The most common predisposing factor in metabolic encephalopathy is liver failure.

Causes and Risk factors

The risk of metabolic encephalopathy is increased with concomitant systemic diseases (e.g., liver cirrhosis, hepatitis, cardiovascular disease, diabetes, renal failure); vitamin B1 deficiency; Hashimoto's thyroiditis; infections; trauma; major surgery; effect of sedatives and narcotics; alcohol intoxication; poisoning (from lead, carbon monoxide, insecticide); sepsis; intestinal bleeding; hypothermia/hyperthermia; electrolyte imbalance (hypo/hypernatremia, hypercalcemia); hypoglycemia; hyperosmolar hyperglycemic crisis; metabolic acidosis; meningitis, encephalitis; and persistent vomiting or diarrhea that lowers blood potassium levels.

Symptoms

Symptoms of metabolic encephalopthy include:

Diagnosis

The symptoms of metabolic encephalopathy are readily recognized by the physician. However, it is also necessary to confirm if other underlying conditions are responsible for the disorder.

Laboratory examinations include complete blood count; blood chemistry; assessment of cerebrospinal fluid (CSF) and blood oxygen concentration. Other confirmatory tests may be prescribed e.g., X-rays, CT scan, MRI, and encephalogram (EEG).

Treatment

Successful treatment of metabolic encephalopathy depends on early recognition of the symptoms and prompt intervention to reverse the conditions that could lead to hypoxia or accumulation of toxins in the bloodstream. Delayed treatment could result in permanent or residual damage to the brain.

Patients are maintained on a low-protein diet to lower blood ammonia levels since ammonia is a by-product of protein metabolism. Comatose patients may required special tube feedings and life support systems.

Liver transplantation may be considered in patients with chronic liver cirrhosis.

References

Article

  1. EFM Wijdicks. Neurologic Complications of Critical Illness. 2004; 8(1):67–68.
  2. Nomoto K, Scurlock C, Bronster D. Dexmedetomidine controls twitch-convulsive syndrome in the course of uremic encephalopathy. J Clin Anesth. 2011 Dec; 23(8):646-8.
  3. Morris Jc, Ferendelli Ja. Metabolic encephalopathy. In:Pearlman AL, Collin RC, eds. Neurobiology of disease. 1990; 496-527.
  4. Jones Ea. Pathogenesis of hepatic encephalopathy. Clin Liver Dis. 2000; 4:467-85.
  5. Norenberg Md. The role of astrocytes in hepatic encephalopathy. Neurochem Pathol. 1987; 6:13.
  6. Pulsinelli WA, Cooper AJ. Metabolic encephalopathies and coma. In GJ Siegel, BW Agranoff, RW Albers and PB Molinoff (eds.), Basic Neurochemistry: Molecular, Cellular and Medical Aspects, 5th ed. 1994; pp. 841–857.
  7. Kirkham FJ. Non-traumatic coma in children. Arch Dis Child. 2001; 85:303.
  8. Parke JT. Acute encephalopathies. In: Oski's Pediatrics. Principles and Practice, 4th ed, McMillan, JA, Feigin, RD, DeAngelis, C, Jones, MD (Eds), Lippincott, Williams & Wilkins, Philadelphia. 2006; p. 2258.
  9. Plum F, Posner JB. The Diagnosis of Stupor and Coma, FA Davis Company, Philadelphia. 1982; p.177.
  10. Wang PS, Schneeweiss S, Avorn J, et al. Risk of death in elderly users of conventional vs. atypical antipsychotic medications. N Engl J Med. 2005; 353:2335-41.
  11. Frontera JA. Delirium and sedation in the ICU. Neurocrit Care. 2011; 14:463-74.

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Last updated: 2018-06-21 22:11