Coma and

A small amount of acrolein may be fatal if swallowed. It produces bums of the mouth, throat, esophagus, and stomach. Signs and symptoms of poisoning may include severe pain in the mouth, throat, chest, and abdomen nausea vomiting, which may contain blood diarrhea weakness and dizziness and coUapse and coma (99). 

Ingestion of large amounts of trichloroethylene may cause Hver damage, kidney malfunction, cardiac arrhythmia, and coma (38) vomiting should not be induced, but medical attention should be obtained immediately. 

The onset of symptoms of barbiturate toxicity may not occur until several hours after the drug is administered. Symptoms of acute toxicity include CNSand respiratory depression, constriction or paralytic dilation of the pupils tachycardia, hypotension, lowered body temperature, oliguria, circulatory collapse, and coma. The nurse should report any symptoms of toxicity to the primary health care provider immediately. 

Although rare, benzodiazepine toxicity may occur from an overdose of the drug. Benzodiazepine toxicity causes sedation, respiratory depression, and coma. Flumazenil (Romazicon) is an antidote (antagonist) for benzodiazepine toxicity and acts to reverse die sedation, respiratory depression, and coma within 6 to 10 minutes after intravenous administration. The dosage is individualized based on the patient s response, widi most patients responding to doses of 0.6 to 1 mg. However, die drug s action is short, and additional doses may be needed. Adverse reactions of flumazenil include agitation, confusion, seizures, and in some cases, symptoms of benzodiazepine withdrawal. Adverse reactions of flumazenil related to the symptoms of benzodiazepine withdrawal are relieved by die administration of die benzodiazepine. 

Use of die MAOIs must be discontinued 2 weeks before the administration of die SSRIs. When the SSRIs are administered witii die tricyclic antidepressants, tiiere is an increased risk of toxic effects and an increased tiierapeutic effect. When sertraline is administered witii a MAOI, a potentially fatal reaction can occur. Sjymptoms of a serious reaction include hyper-tiiermia, rigidity, autonomic instability witii fluctuating vital signs and agitation, delirium, and coma Sertraline blood levels are increased when administered witii cimetidine. 

When dextromethorphan is administered with the monoamine oxidase inhibitors (see Chap. 31), patients may experience hypotension, fever, nausea, jerking motions to the leg, and coma... 

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. 

Finally, we return to our example of a two mode turbulence, tilt and coma, with a single measurement of the centroid displacement, d. We assume, for simplicity, that there is no noise on the measurements, hence = 0. If we as-... 

Unfortunately, there is not a linear relationship between the light intensity in the measurement plane and the wavefront. This is shown in Fig. 2 which shows the intensities measured at the focal plane for a wavefront equal to pure tilt and coma terms individually. It is apparent that scaling the wavefront by a (in this case 5) does not result in a linear increase in the measured intensity by a factor a. The key difference between existing existing wavefront sensors such as the Shack-Hartmann, curvature and pyramid sensors is how they transform the measured intensity data to produce a linear relationship between the measurements and the wavefront. 

One of six workers died 12 days after exposure to a mixture of half dimethyltin dichloride and half trimeth-yltin chloride vapour during cleaning of a cauldron at a chemical plant in Germany in 1981. Maximum exposure time was 1.5 h over a 3-day period no estimates of exposure concentration were made. Symptoms preceding death included excretion of high levels of tin in the urine, respiratory depression, and coma (Rey et al.,... 

Mutation of the dihydrolipoate reductase component impairs decarboxylation of branched-chain a-keto acids, of pyruvate, and of a-ketoglutarate. In intermittent branched-chain ketonuria, the a-keto acid decarboxylase retains some activity, and symptoms occur later in life. The impaired enzyme in isovaleric acidemia is isovaleryl-CoA dehydrogenase (reaction 3, Figure 30-19). Vomiting, acidosis, and coma follow ingestion of excess protein. Accumulated... 

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 fulminant hepatitis with hepatic encephalopathy, patients may have asterixis and coma. 

TBW depletion (often referred to as dehydration ) is typically a more gradual, chronic problem compared to ECF depletion. Because TBW depletion represents a loss of hypotonic fluid (proportionally more water is lost than sodium) from all body compartments, a primary disturbance of osmolality is usually seen. The signs and symptoms of TBW depletion include CNS disturbances (mental status changes, seizures, and coma), excessive thirst, dry mucous membranes, decreased skin turgor, elevated serum sodium, increased plasma osmolality, concentrated urine, and acute weight loss. Common causes of TBW depletion include insufficient oral intake, excessive insensible losses, diabetes insipidus, excessive osmotic diuresis, and impaired renal concentrating mechanisms. Long-term care residents are frequently admitted to the acute care hospital with TBW depletion secondary to lack of adequate oral intake, often with concurrent excessive insensible losses. 

Hyponatremia is very common in hospitalized patients and is defined as a serum sodium concentration below 136 mEq/L (136 mmol/L). Clinical signs and symptoms appear at concentrations below 120 mEq/L (120 mmol/L) and typically consist of agitation, fatigue, headache, muscle cramps, and nausea. With profound hyponatremia (less than 110 mEq/L [110 mmol/L]), confusion, seizures, and coma maybe seen. Because therapy is also influenced by volume status, hyponatremia is further defined as (1) hypertonic hyponatremia (2) hypotonic hyponatremia with an increased ECF volume (3) hypotonic hyponatremia with a normal ECF volume and (4) hypotonic hyponatremia with a decreased ECF volume.16... 

Mood lability, inappropriate aggressive or sexual behavior, giddiness or verbally loud, impaired judgment possibly progressing to somnolence and coma as the blood level increases... 

Complications of falciparum malaria include hypoglycemia, acute renal failure, pulmonary edema, seizure, and coma. 

Central nervous system confusion, headache, lethargy, seizures, and coma... 

Data on the NOAELS and LOAELS for death are presented in Table 2-1 for several animal species. The data presented indicate that species differences exist with respect to acute lethal effects. Dogs appear to be the most susceptible species, but this is based on studies involving only a few animals. The cause of death varied among test species. In guinea pigs, death resulted from pulmonary irritation (see Section 2.2.1.2) while in the other species convulsions and coma occurred (see Section 2.2.1.4) (Dudley and Neal 1942). It should be noted that this study is based on nominal concentrations without analytical verification. 

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