Barbiturates barbiturate coma

Barbiturates. Barbiturates—which produce a wide spectrum of CNS depression, from mild sedation to coma—have been used as sedatives, hypnotics, anesthetics, and anticonvulsants since they were first introduced for medical use in the early 1900s. 

Schwab S., Spranger M., Schwarz S., and Hacke W. (1997) Barbiturate coma in severe hemispheric stroke useful or obsolete Neurology 48, 1608-1613. 

Life-threatening hyperkalemia after therapeutic barbiturate coma with thiopental has been described in three patients it was fatal in one (6). All the episodes occurred after the withdrawal of thiopental. Hypokalemia that is resistant to potassium replacement is common during thiopental coma and clinicians may choose to manage asjmptomatic barbiturate-induced hypokalemia expectantly in an attempt to avoid rebound hyperkalemia. 

Cairns CJ, Thomas B, Fletcher S, Parr MJ, Finfer SR. Life-threatening hyperkalaemia following therapeutic barbiturate coma. Intensive Care Med 2002 28(9) 1357-60. 

Treat insomnia use for sedation, preoperative medication, barbiturate coma (for controlled increased intracranial pressure)... 

Prior to indncing a barbiturate coma, the severe TBI patient mnst be mechanically ventilated with continuous monitoring of arterial... 

Most reports in the clinical literature recommend stopping the convulsion within 1 hour, using drastic measures, such as hypothermia and barbiturate coma, if necessary.108 The mortality of status epilep-ticus (usually defined as a convulsion lasting 60 min, or a series of convulsions lasting 60 min without consciousness intervening) is said to be 6% to 30%. Moreover, twice that number of victims acquire irreversible neurological deficits as a result of status epilepticus.108 (In a study of children, permanent deficits were found to occur in 34%.109) These data emphasize the need for an effective anticonvulsant. 

Orlowski JP, Erenberg G, Lueders H, Cruse RP. Hypothermia and barbiturate coma for refractory status epilepticus. Crit Care Med. 1984 12 367-372. 

A. Specific levels of phenobarbital are usually readily available from hospital clinical laboratories concentrations greater an 60-80 mg/L are usually associated with coma and those greater than 150-200 mg/L with severe hypotension. For short- and intermediate-acting barbiturates, coma is likely when the semm concentration exceeds 20-30 mg/L. Barbiturates are easily detected in routine urine toxicologic screening. 

Administer supplemental oxygen, and treat bronchospasm (see p 8), pulmonary edema (p 7), seizures (p 22), and coma (p 19) if they occur. Intractable seizures usually predict a fatal outcome. Consider induction of barbiturate coma with a short-acting agent such as pentobarbital (p 485) and consult a neurologist as soon as possible. 

Ng SY, Chin KJ, Kwek I K. Dyskalaemia associated with thiopentone barbiturate coma for refractory intracranial hifperten-sion a case series. Intensive Care Med 2011 37 1285-9. 

Gastrointestinal There have been two reports of bowel ischemia after barbiturate coma treatment for refractory status epilep-ticus [91 ]. 

Electrolyte balance Disturbances of potassium homeostasis rarely complicate therapeutic barbiturate coma [92 ]. 

Neil Ml, Dale MC. Hypokalaemia with severe rebound h3rperkalaemia after therapeutic barbiturate coma. Anesth Analg 2009 108(6) 1867-8. 

All barbiturates have essentially die same mode of action. Depending on the dose given, tiiese drags are capable of producing central nervous system (CNS) depression and mood alteration ranging from mild excitation to mild sedation, hypnosis (sleep), and deep coma These drugs also are respiratory depressants the degree of depression... 

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. 

Death from overdose of barbiturates may occur and is more likely when more than 10 times the hypnotic dose is ingested. The barbiturates with high lipid solubility and short half-lives are the most toxic. Thus the lethal dose of phenobarbital is 6—10 g, whereas that of secobarbital, pentobarbital, or amo-barbital is 2-3 g. Symptoms of barbiturate poisoning include CNS depression, coma, depressed reflex activity, a positive Babinski reflex, contracted pupils (with hypoxia there may be paralytic dilation), altered respiration, hypothermia, depressed cardiac function, hypotension, shock, pulmonary complications, and renal failure. 

The side effects of barbiturates include sedation, poor physical coordination, and impaired mental performance. They also potentiate the intoxicating effects of alcohol. Barbiturates can be extremely dangerous in overdose, causing anesthesia, coma, and even death. In addition, barbiturates can cause dangerous suppression of breathing in patients with sleep apnea or other respiratory disorders. With repeated use over just a few weeks, physical dependence and tolerance to their effects can develop, leading to increasing doses to maintain the desired therapeutic effect. If a... 

In humans, early symptoms of intoxication may include headache, dizziness, nausea, vomiting, malaise, and myoclonic jerks of the limbs clonic and tonic convulsions and sometimes coma follow and may occur without the premonitory symptoms. A suicidal person who ingested 25.6mg/kg developed convulsions within 20 minutes that persisted recurrently until large amounts of barbiturates had been administered. Hematuria and azotemia occurred the day after ingestion and continued for 18 days. Liver function studies were within normal limits except for an elevated icterus index an electroencephalogram revealed generalized cerebral dysrhythmia, which returned to normal after 5 months. ... 

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. 

Diazepam (Valium, Diastat) [C-IVj [Anxiolytic, Skeletal Muscle Relaxant, Anticonvulsant, Sedative/Hypnotic/ Benzodiazepine] Uses Anxiety, EtOH withdrawal, muscle spasm, status epilepticus, panic disorders, amnesia, preprocedure sedation Action Benzodiazepine Dose Adults. Status epilepticus 5-10 mg IV/IM Anxiety 2-5 mg IM/IV Preprocedure 5-10 mg IV just prior to procedure Peds. Status epilepticus 0.5-2 mg IV/IM Sedation 0.2-0.5 mg/kg IV (onset w/in 5IV and 30 min IM duration about 1 h IV and IM) Caution [D, / -] Contra Coma, CNS depression, resp d es-sion, NAG, severe uncontrolled pain, PRG Disp Tabs 2, 5, 10 mg soln 1, 5 mg/mL inj 5 mg/mL rectal gel 2.5, 5, 10, 20 mg/mL SE Sedation, amnesia, bradycardia, i BP, rash, X resp rate Interactions T Effects W/ antihistamines, azole antifungals, BBs, CNS depressants, cimetidine, ciprofloxin, disulfiram, INH, OCP, omeprazole, phenytoin, valproic acid, verapamil, EtOH, kava kava, valman T effects OF digoxin, diuretics X effects w/ barbiturates, carbamazepine. 

Pentobarbital (Nembutal, Others) [C-ll] [Anticonvulsant, Sedative/ Hypnotic/Barbiturate] Uses Insomnia, convulsions, induce coma following severe head injury Action Barbiturate Dose Adults. Sedative ... 

Coma Decrease Dilated Hypothermia Barbiturates or other sedatives... 

Phenobarbitai is a very sedative barbiturate, with a iong eiimination haif-iife. It can cause drowsiness, coma, and respiratory depression. It is therefore safe to use it only where adequate facilities are available for mechanical ventilation if that is required. Sodium valproate infusion has been shown to be effective in children with status in a small uncontrolled study. 

Kava should not be used with alcohol, benzodiazepines, barbiturates or other sedatives because of their additive effects. In one case, coma resulted from mixing alprazolam and kava. Patients have complained that kava, while relaxing the body, may be less effective for mental anxiety with obsessive or racing thoughts than are the benzodiazepines. 

Historically, alcohol has been used as an anxiety-reducing agent, both casually and in professional medical settings. In 1903, barbital was introduced as the first barbiturate to treat anxiety, and phenobarbital followed a few years later. Barbiturates have many side effects and addictive properties, and overdose can lead to coma and death. For these reasons, they are rarely used today, except to treat some forms of epilepsy. This class of drugs was eventually replaced by the benzodiazepines (see Chapter 4). 

GNS depressants are drugs that decrease brain activity, resulting in both behavioral and physiological changes. The effects of alcohol on coordination, speech, and cognitive functions are familiar to most people. The effects of barbiturates are similar to alcohol. In low doses, barbiturates act as sedatives increased doses have a hypnotic or sleep-inducing effect and stiU larger doses have anticonvulsant and anesthetic activity, and can lead to respiratory depression, coma, and death. Barbiturate addicts... 

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