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Toxic-Metabolic Encephalopathies Definition Group of neurological disorders whose hallmark is an altered mental status Caused by failure of organs other than nervous system or presence of an endogenous or exogenous toxin or drug BBB isolate brain Multifocal cortical disorder Delirium A confusional state with superimposed hyperactivity of the sympathetic limb of the autonomic nervous system with consequent signs including tremor, tachycardia, diaphoresis, and mydriasis Confusion: inability to maintain a coherent stream of thought or action TME Acute toxic-metabolic encephalopathy (TME): encompasses delirium and the acute confusional state Acute condition of global cerebral dysfunction in the absence of primary structural brain disease TME common among critically ill patients probably underrecognized and undertreated Most TME is reversible, making prompt recognition and treatment important Certain metabolic encephalopathies, including those caused by sustained hypoglycemia and thiamine deficiency (Wernicke's encephalopathy), may result in permanent structural brain damage if untreated Clinical manifestations Mental status abnormalities :range from subtle to deep coma Impaired orientation, cognition, memory, affect, perception , judgement Pupils: sluggish, small, irregular Eye movement: disconjugate gaze Motor: increase in tone Spasticity with extensor plantar response Pathophysiology Normal neuronal activity requires a balanced environment of electrolytes, water, amino acids, excitatory and inhibitory neurotransmitters, and metabolic substrates normal blood flow, normal temperature, normal osmolality, and physiologic pH are required for optimal central nervous system function Pathophysiology All forms of acute toxic-metabolic encephalopathy (TME) interfere with the function of the ascending reticular activating system and/or its projections to the cerebral cortex, leading to impairment of arousal and/or awareness Ultimately, the neurophysiologic mechanisms of TME include interruption of polysynaptic pathways and altered excitatory-inhibitory amino acid balance Increased permeability of the blood-brain barrier is evidenced by elevated protein in the CSF, a frequent finding in TME Pathophysiology The pathophysiology of TME varies according to the underlying etiology: Cerebral edema contributes to acute fulminant hepatic encephalopathy and to hypoosmolar encephalopathies Drug-induced delirium results from disruption of the normal integration of neurotransmitters, including dopamine, acetylcholine, glutamate, gamma-aminobutyric acid (GABA), and/or serotonin Electrolyte derangements alter membrane excitability Nutritional disorders disturb cellular energy metabolism and may result in neuronal death Exogenous toxins, including carbon monoxide and cyanide, cause impaired oxygen delivery and mitochondrial dysfunction Clinical findings Mltifocal myoclonus Cramps Trousseau’s sign Tremors Weakness Asterixis Generalized, focal, myoclonic seizures Hepatic encephalopathy Liver disease causes encephalopathy by 2 mechanisms : 1-Hepatocellular failure 2-Diversion of toxins from hepatic portal vein into the systemic circulation Precipitating factors GI bleed Drug induced Excess dietary protein Hypokalmeia Constipation infections Toxin hypersensitivity : patients becoming more susceptible to effect of precipitants Portal systemic encephalopathy: cirrhosis with shunts Pathogenesis The most important factors in the pathogenesis are: 1-severe hepatocellular dysfunction and/or intrahepatic and extrahepatic shunting of blood into the systemic circulation so that the liver is largely bypassed. 2- Various toxic substances absorbed by the intestine are not detoxified by the liver and lead to metabolic abnormalities in the CNS. Ammonia is the substance most often incriminated in the pathogenesis of encephalopathy. Others include mercaptans, short- chain fatty acids and phenols. Uremic encephalopathy Coexistence of signs of nervous system depression (obtundation) and neural excitation (twitching, myoclonus, agitation and seizures) Dut to: Progressive azotemia Effect of treatment :dialysis disequilibrium syndrome, dementia from aluminum accumulation Complication of transplantation and immunosupression Disorders of glucose metabolism Hypoglycemia Non-ketotic hyperosmolar coma DKA B12 deficiency Early : cognitive changes Late : dementia ,optic atrophy Irreversible if not treated early Sub-acute combined degeneration of spinal cord Wernicke-Korsakoff encephalopathy Chronic alcoholism Hyperemesis gravidarum Malignancy GI surgery HD Prolonged intravenous feeding Anorexia nervosa AIDS Wernicke-Korsakoff encephalopathy Triad of : Confusion Opthalmoplegia Ataxia Pathology : small hemorrhages in periventricular grey matter around aqueduct,3rd and 4th ventricles Treatment : Thiamine glucose Central pontine myelinolysis Caused by rapid osmotic change Rapid correction of sodium Rule : no more than 12 mmol per liter per 24 hrs Clinically : flaccid or spastic quadreplegia Psuedobulbar palsy Decrease LOC Toxic encephalopathies 6 groups: Alcohol BZD Salicylaytes Acetaminophen Barbiturates TCA’s Hypoxic-ischemic encephalopathy brain utilizes oxygen to metabolize glucose. It cannot store oxygen and survives only for minutes after its oxygen supply is reduced below critical levels. Pyramidal cells in Sommer's sector of the hippocampus, Purkinje cells of the cerebellum, and pyramidal cells of the third and fifth layers of the cerebral cortex are vulnerable to even moderate degrees of anoxia HIE Anoxic anoxia consists of low arterial oxygen content and tension. This may be secondary to decreased oxygen in the environment or inability for oxygen to enter the circulatory system as in pulmonary disease Anemic anoxia consists of low oxygen content in the blood secondary to decreased hemoglobin content. Ischemic anoxia describes a state of insufficient cerebral blood flow. "Low-flow states" may be secondary to cardiovascular collapse or conditions of increased vascular resistance as in stroke or migraine HIE Result from a number of conditions such as: Cardiac arrest CO intoxication Septic shock HIE Spectrum : Syncope : breif global cerebral ischemic anoxia Focal cerebral ischemia : hypotension leading to watershed infraction Postanoxic coma Persistent vegetative state Cerebral edema Delayed postanoxic deterioration Brain death Irreversible cessation of CNS function Diagnosis based on absence of all cerebral and brainstem functions persisteng over a peroid of observation suffeicent to exclude any possibilty of recovery Prognosis and Complications post-arrest coma longer than three days carried an unfavorable prognosis Individuals with the best chance of recovery had preserved brainstem function following the initial insult Management Diagnostic difficulty: drugs, sepsis Continuos monitoring Watch for complications: NCSE CT brain LP EEG Management No known specific treatment that reverse AIE Rapid re-establishing circulation Normal or somewhat increased BP Normal ABG Control hyperthermia and seizures AED :if indicated