Coma manifestation

Portacaval-shunted rats administered ammonium salts to precipitate coma manifest impaired brain energy metabolism (Hindfelt et al., 1977). Possible mechanisms responsible for this include inhibitory effects of ammonia on the tricarboxylic acid... 

Bccesave dosage is manifested as water intoxication (fluid overload). Symptoms of water intoxication include drowsiness, listlessness confusion, and headache (which may precede convulsions and coma). If sgns of excessive dosage occur, the nurse should notify the primary health care provider before the next dose of the drug is due because a change in the dosage, the restriction of oral or IV fluids and the administration of a diuretic may be necessary. 

There is ample precedent for a modulatory role of K channels in behavior. The K channel blocker, 4-AP, selectively blocks component T (Bartschat and Blaustein 1985a). prolongs nerve action potentials, and enhances neurotransmitter release (Llinas et al. 1975). In man, intoxication with this agent may lead to dissociative behavior, agitation, confusion, convulsions, and coma (Spyker et al. 1980). However, the behavioral aberrations induced by 4-AP differ qualitatively from those induced by PCP. This implies that block of various types of presynaptic K channels may modify behavior and mental activity however, the precise nature of the behavioral manifestations is likely to depend upon the specific type of K channel that is affected. 

In adult patients, the manifestations of PCP use can be grouped into nine clinical patterns of intoxication. Four of these are called major patterns because they may be associated with severe toxicity and often necessitate hospitalization. Patients with major patterns are usually unpredictable symptoms wax and wane, and the patient may abruptly change from one pattern of intoxication to another. Five other symptom complexes are designated as minor patterns since toxicity is usually mild and of short duration. Major Patterns consist of coma, catatonic syndrome, toxic psychosis, and acute brain syndrome. Minor Patterns are lethargy, bizarre behavior, violent behavior, agitation, and euphoria (McCarron et al. 1981b). 

Uremic and dialysis encephalopathies. Patients with renal failure continue to manifest neuropsychiatric symptoms despite significant advances in therapeutics and management. Patients with renal failure who are not yet on dialysis develop an array of symptoms, including clouding of consciousness, disturbed sleep patterns, tremor and asterixis that may progress to coma and death. 

Infants are protected during gestation because the placenta clears most potential toxins. The classical form of the disease therefore does not become clinically manifest until a few days after birth. An initial phase of alternating irritability and lethargy progresses over a period of days to frank coma and respiratory embarrassment. Irreversible brain damage is common in babies who survive, particularly those whose treatment is delayed until after the first week of life. 

Severe urea cycle defects become manifest in infants with a severe syndrome of coma, convulsions and vomiting during the first few days of life. Clinical confusion with septicemia is common, and many infants are treated futilely with antibiotics. Hyperammonemia is usually severe, even in excess of 1 mmol/1 (normal in term infants <100 xmol/l). 

Lysinuric protein intolerance. Infants manifest growth failure, hepatosplenomegaly, vomiting, hypotonia, recurrent lethargy, coma, abdominal pain and, in rare instances,... 

Fructose-1,6-bisphosphatase deficiency, first describ ed by Baker and Winegrad in 1970, has now been reported in approximately 30 cases. It is more common in women and is inherited as an autosomal recessive disorder. Initial manifestations are not strikingly dissimilar from those of glucose-6-phosphatase deficiency. Neonatal hypoglycemia is a common presenting feature, associated with profound metabolic acidosis, irritability or coma, apneic spells, dyspnea, tachycardia, hypotonia and moderate hepatomegaly. Lactate, alanine, uric acid and ketone bodies are elevated in the blood and urine [11]. The enzyme is deficient in liver, kidney, jejunum and leukocytes. Muscle fructose-1,6-bisphosphatase activity is normal. 

Myxedema coma is a rare consequence of decompensated hypothyroidism manifested by hypothermia, advanced stages of hypothyroid symptoms, and altered sensorium ranging from delirium to coma. Untreated disease is associated with a high mortality rate. 

Neurologic manifestations of severe hypophosphatemia include a progressive syndrome of irritability, apprehension, weakness, numbness, paresthesias, dysarthria, confusion, obtundation, seizures, and coma. 

The first group persons in grave condition threatening their life (acute respiratory failure and cardiovascular collapse, coma, convulsions, paralytic manifestations). Upon first aid provided, these persons are to be evacuated to specialized medical institutions as soon as possible, preferably by ambulance cars, equipped with reanimation facilities. 

The clinical picture of carbaryl intoxication results from inactivation of cholinesterase, resulting in the accumulation of acetylcholine at synapses in the nervous system, skeletal and smooth muscle, and secretory glands. Signs and symptoms of overexposure may include (1) muscarinic manifestations such as miosis, blurred vision, lacrimation, excessive nasal discharge or salivation, sweating, abdominal cramps, nausea, vomiting, and diarrhea (2) nicotinic manifestations including fasiculation of fine muscles and tachycardia and (3) central nervous system manifestations characterized by headache, dizziness, mental confusion, convulsions, coma, and depression of the respiratory center. 

Toxic symptoms may be dose-dependent and merely an exaggeration of the therapeutically desirable response, e.g., the coma of barbiturate overdosage and persistence of muscular paralysis after succinylcholine administration, or an unpredictable effect of the drug upon an organ or tissue remote from that upon which the therapeutic effect is manifested. 

Hepatic function impairment In patients with preexisting severe liver disease, hepatic encephalopathy (manifested by tremors, confusion, and coma, and increased jaundice) may occur. Because amiloride is not metabolized by the liver, drug accumulation is not anticipated in patients with hepatic dysfunction, but accumulation can occur if hepatorenal syndrome develops. 

Neurologic - A transient acute neurologic syndrome has been observed in patients treated with high-dosage regimens. Manifestations of this stroke-like encephalopathy may include confusion, hemiparesis, transient blindness, seizures, and coma. 

These effects lead to major clinical manifestations, including nausea, vomiting, dehydration, electrolyte imbalance, loss of consciousness and, potentially, coma and death. 

The most extreme manifestation of untreated hypothyroidism is myxedema coma, which even if detected early and appropriately treated, carries a mortality rate of 30 to 60%. Myxedema coma is a misnomer. Most patients exhibit neither the myxedema nor coma. Patients with myxedema coma usually have longstanding hypothyroidism with the classic symptoms of hypothyroidism. Decompensation into myxedema coma may occur when the homeostatic mechanisms of the severely hypothyroid patient are subject to a stressful precipitating event (e.g., infection, trauma, some medications, stroke, surgery). The principal manifestation of myxedema coma is a deterioration of mental status (apathy, confusion, psychosis, but rarely coma). Other common clinical features include hypothermia, diastolic hypertension (early), hypotension (late), hypoventilation, hypoglycemia, and hyponatremia. If myxedema coma is suspected, the patient is usually admitted to an intensive care unit for pulmonary and cardiovascular support... 

Severe anticholinergic reaction, manifested by severe lethargy, hypotonic reflexes, and hyperthermia, may result in severe respiratory depression and coma. 

Ethanol and sedative hypnotic intoxication are both characterized by behavioral disinhibition, which can be manifested as inappropriate aggressive or sexual behavior, mood lability, and impaired judgement. Associated signs include slurred speech, incoordination, unsteady gait, nystagmus, and impaired attention and memory. Ingestion of excessive amounts can result in stupor, coma, and death from respiratory depression. 

Carbamazepine toxicity is manifested by drowsiness, nausea and vomiting, gait disturbance, nystagmus, confusion, neuromuscular excitability, and seizures (Menkes, 1999). Overdose with CBZ can be lethal (Arana et ah, 1986). In a retrospective study of 307 intoxicated patients, 41 (13%) had a fatal outcome (Schmidt and Schmitz-Buhl, 1995). Doses exceeding 24 g were important indicators of fatality. The management of CBZ overdose is primarily supportive, to prevent potential atrioventricular (AV) block (Arana et ah, 1986), possible respiratory depression (Schmidt and Schmitz-Buhl, 1995), stupor, and coma. 

Valproate overdose results in increasing sedation, confusion, and ultimately, coma. The patient may also manifest hyperreflexia or hyporeflexia, seizures, respiratory suppression, and supraventricular tachycardia. Treatment should include gastric lavage, electrocardiographic monitoring, treatment of emergent seizures, and respiratory support. 

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