Cocaine overdose management

java · Consumer

Note : This thread was generated at the Hive following an incident with a hive seeking help at the forum, the following are comments and sugestions from the members......java

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wareami
(Hive Addict)
11-07-04 21:33
No 540327




Hosptal EMS time!
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Cocaine Kills!
Nothing to do but call for immediate EMS help.
That's 911 in US.
No home remedy...no poison control center.
If symptoms haven't fully developed then they could call poison control for interim medical advice until ambulance arrives.
Heart attack or stroke are serious risks within three days after cocaine overdose.
There is no, Don't GO in this case!

If the shoethrows fits...Ware Itout

wareami
(Hive Addict)
11-07-04 21:46
No 540328




That really sucks...
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But that is the only remedy.
Noone would be seeking this info for themselves!
Ibees stood on that threshold a few times and he was too kooked to care about help, although it did scare the shit out of him....there was nothing he could do!
That's why I say this must be for someone other than the poster.
Ibee followed up with medical treatment after the worst case because his chest felt like it would cave in the next day!
No LE was involved at the ER and they just treated it as potential cardiac arrest...ran tests and released.
Ibee told the ER techs what had occured!
This is a fine line between life and death and never would I suggest anybee set themselves UP for a fall.
But even if this was a close call and the patient recovers....he's still in danger if the amount consumed or the %age was high.

If the shoethrows fits...Ware Itout

LaBTop
(Daddy)
11-07-04 21:47
No 540329




Victim is hopefully
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already in hospital.

Question: In case of a cocaine overdose, the user should best and as quickly as possible swallow sleeping medicines or tranquillizers.
Answer: Incorrect. The agitation that comes with an overdose of cocaine could indeed be combatted with benzodiazepines but the individual should better not selfmedicate with benzodiazepines. Due to the slow absorption by the blood the effect of sleeping medicines and tranquillizers is delayed. In a panic situation, the person might easily take too many pills and suppress his/her breathing.

8. A cocaine overdose can cause a heart attack.
Correct. An overdose of cocaine can manifest itself in two ways: 1. chest pains and 2. epileptic attacks. In the first case, heartbeat and blood pressure rise rapidly, which can lead to a heart attack.

9. During an epileptic attack due to a cocaine overdose, you must try to keep open the mouth by inserting an object.
Incorrect. Putting something in the mouth does not help and might cost the helper a few fingers. It is also not too good for the teeth of the victim. Better call an emergency number and protect the heavily convulsing victim by laying him somewhere on the ground where he cannot get hurt. Put a pillow or jacket under his head. When the convulsions have stopped, put him in a side position with the upper leg bent and the lower leg straight, the head straight or slightly bent backward.

10. The combination of heroin and benzodiazepines increases the chance of a cocaine overdose.
Correct. With heroin and benzodiazepines in his blood, the cocaine user feels very relaxed, which makes a second helping of cocaine very tempting. The relaxation, however, is only pretence. In reality, the heart is doing overtime and the next 'line' could well be the last.

http://www.drugtext.org/library/books/_vti_bin/shtml.dll/raterisks/4.2.htm

Looking for more, but surprisingly little to find in short time, when the best info can be life saving. Damn, lots of these sites want you to login etc, idiots! LT/

WISDOMwillWIN

Xaja
(Hive Bee)
11-07-04 21:47
No 540331




Hey
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Cocaine overdose is treated as a medical emergency. Sedation with agents such as diazepam (Valium) is recommended for the agitation, irritability, seizures, and hyperexcitable state. This also helps control the rapid heart rate and elevated blood pressure. If the body temperature is elevated, this is brought down with cold water, fans, cooling blankets, and acetaminophen (Tylenol). Specific therapies are geared to the specific complaint or system involved. For example, if the cocaine overdose has led to a true heart attack, clot-dissolving medications called thrombolytic drugs may be used. Further testing with a cardiac catheterization (a test that places a long catheter in the leg artery to take pictures of the heart's arteries to see if they are blocked) may be done. If this test shows a blocked vessel, a balloon angioplasty (a procedure using a small balloon to open up the blocked artery) may also be done. Treatment depends on the presenting complaint and organ system involved.

Get them to an ER immediately!!!

**FriedPiper**

>>This is my signature.<<

methyl_ethyl
(Guardian)
11-07-04 21:58
No 540333




I don't care where you live
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It doesn't matter where you live, there is not much you can do at your house to prevent multiple organ failure. The pathophysiology associated with cocaine overdose is very complicated and involves almost every organ system.

Make sure you can maintain an airway, monitor cardiac output, hopefully you are familiar with rescue breathing, or CPR if needed. Beta Blockers can be used, along with benzo's if you have access to them and know what you are doing, (I assume you do not as you are looking for help online) Make sure you tell Emergency Services EVERYTHING!!! what they took, what you did in order to keep them alive up to now, i.e. if you administered beta blockers, or gave them ANYTHING to counter their symptoms. Inform emergency services of their breathing rate, pulse, temperature, general appearence, anything that will let them know what they are in for.

There should be a sticky thread on OD'ing that states, if you think someone is OD'ing the last place in the world you should look for information is the hive. That being said we should compile some information as to what bees can do until help arrives, or the victom is brought to the hospital. Sort of a preventative measure, if everyone has a good grasp as to what to do before something like this happens perhaps the crisis can be minimized to an extent.

I will try to do what I can in the future but that does not help anyone out now

I hope to hell Quality you are not still in front of your computer screen....

m_e

   Unipolar Mania, It's good for life...

New: Post 12 of 12

Subject: Cocaine overdose management

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LaBTop
(Daddy)
11-07-04 22:16
No 540341




Survivors guide
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http://www.drugtext.org/sub/parents/survivors%20guide.htm

a survivor's guide

There are many drugs available and when mixed together they can cause all sorts of complex reactions within the body. Some can make people very drowsy, others can lead to people being very tense and panicky. Some drugs have caused people to overheat and become severely dehydrated. In some situations people can take too much or have a bad reaction to a drug and fall unconscious.

What follows are some guidelines for administering basic first aid..

Do you know how to..

Take someone's pulse?

Give mouth to mouth resuscitation?

Place somebody in the recovery position?

Save lives?

If people are tense and panicky..

This can occur with many drugs including hallucinogenic drugs like LSD and magic mushrooms, but it also happens with upper drugs like amphetamines and ecstasy as well as with high doses of cannabis. If someone is really tense and panicky on drugs, take the following steps:

Calm them down and reassure them.

Establish what drugs have been taken.

Talk quietly and explain that the panicky feeling will gradually go as the effect of the drug wears off.

Keep them away from loud noises and bright lights and overly inquisitive spectators.

Help them if they hyperventilate. When someone breathes very quickly and gasps for breath, they often get dizzy and feel sick. This can be alleviated by getting the person to breath evenly into a paper bag. This will help calm the person down and restore a normal pattern of breathing.

If people faint or lose consciousness..

First aid for drug overdose is essentially the same as for any unconscious person. This can happen with downer drugs like alcohol, heroin and tranquillisers but is also common with solvents (glue and gas) and poppers and can happen to people who react badly or overheat on amphetamine or ecstasy.

If this happens take the following steps:

Call 999 for medical assistance.
Check their breathing.
If they are not breathing, be prepared to do mouth-to-mouth resuscitation.
If they are breathing, place the person in the recovery position.

Loosen any tight clothing that might restrict their breathing.

Never let a sleepy or unconscious person to drink or be sick.

Keep them warm by use of blankets or a coat (but not too warm). This does not apply if loss of consciousness is caused by overheating.

When the ambulance crew arrives, give them as much information as you can, such as which drugs have been taken, when, etc.

If people are drowsy but conscious..

If someone is really drowsy take the following steps:

Check they are breathing. If so, place the person in the recovery position and keep talking to them.

Don't put them to bed (People have been put to bed in a drowsy state only to be found dead the next morning).

Talk to them, stay with them.

DO NOT give any drinks.

Call 999 for medical assistance if necessary!



If people overheat or dehydrate..

This tends to happen with drugs like amphetamine and ecstasy when people physically exert themselves. These drugs raise body temperature especially if people use them whilst dancing in hot places, like night clubs.

The warning signs include..

Cramps in the legs, arms and back.

Failure to sweat.

Headaches, dizziness and vomiting.

Suddenly feeling very tired.

Feeling like needing the toilet but not doing much when you go (urine becomes too concentrated).

Fainting.



It can be prevented by..

Avoiding amphetamine or ecstasy in the first place. Not dancing for long periods of time.

Talking regular rests and resting in a cool area.

Drinking water, fruit juice or a sports drink at about the rate of one pint an hour (no more), sipping the drink regularly and avoiding alcohol.

Drinking or eating something that keeps the salt levels in the body up. Salty snacks, fruit juice, fizzy drinks and sports drinks will all help to keep the body provided with the minerals it needs.

Wearing cool clothes and not wearing a cap will help.



If someone is overheating.*

Call 999 for medical assistance.

Move the person to a cool area - possibly outside.

Move them to an air-conditioned room if possible and stay with them. People who overheat may have a fit or pass out.

Administer cool, non-alcoholic drinks if conscious.

Splash them down with luke warm water to cool them down, cover in wet cool sheets and/or fan them.

WISDOMwillWIN

methyl_ethyl · Riedel De Haen

great start java,

If y'all think it would be useful I can post the complete Micromedex "poisondex" reference for Cocaine (or any other drug for that matter). There is so much information I fear that it would be overwhelming however, not to mention take up lots of space. I am sure you computer folks could assist me in compressing each individual drug index into a small file that can be accessed if so needed. The information may be exhaustive in nature however it may be invaluable in the case of a life threataning situation. Perhaps if we had time we could extract the pertinent information from these indexes that would more than likely be useful to the recreational users. For example Cocaine has the following subject headings in Poisindex,

COCAINE

* OVERVIEW
* SUBSTANCES INCLUDED/SYNONYMS [+]
* CLINICAL EFFECTS [+]
* LABORATORY/MONITORING [+]
* ABSTRACTS
* TREATMENT [+]
* RANGE OF TOXICITY [+]
* KINETICS [+]
* PHARMACOLOGY/TOXICOLOGY [+]
* PHYSICOCHEMICAL [+]
* ANIMAL TOXICOLOGY [+]
* REFERENCES

To give you an idea of the comprehensive nature of the information found within poisindex I will post an excerpt from the Treatment subject heading...

-- 6.0 TREATMENT

* 6.1 LIFE SUPPORT
o A) Support respiratory and cardiovascular function.

* 6.3 PATIENT DISPOSITION
o 6.3.1 DISPOSITION/ORAL EXPOSURE
+ 6.3.1.1 ADMISSION CRITERIA/ORAL
-- A) Patients with serious end organ effects from cocaine abuse including persistent alteration of mental status, significant hyperthermia or rhabdomyolysis, coagulopathy, metabolic acidosis, severe hypertension, chest pain suggestive of myocardial ischemia, or renal or hepatic failure require intensive care admission.
-- B) Because of the risk of cocaine packet rupture which may be lethal, all body packers must be hospitalized for diagnostic tests and evacuation of the ingested packets, vials, or condoms.
-- C) In the absence of information regarding the type of packaging, even asymptomatic body packers should be admitted to the intensive care unit.

+ 6.3.1.2 HOME CRITERIA/ORAL
-- A) A patient with agitation, mild tachycardia, or hypertension which resolves with observation or minimal medical therapy may be discharged with referral for drug abuse counseling.
-- B) Body packers may be discharged when all packets have been passed. This process may take several days and may require repeated barium enhanced abdominal radiographs or CT to document evacuation of all packets (Hoffman et al, 1990).

+ 6.3.1.5 OBSERVATION CRITERIA/ORAL
-- A) In a prospective, cohort study, 302 patients with cocaine-associated chest pain (by report or urine drug screen) were admitted to an observation unit and treated with aspirin (93% of patients), nitrates (90% of patients), and benzodiazepines (30% of patients). The duration of chest pain was less than 6 hours in 59% (n=171 of 290 patients) of patients; 41% (n=118) had no pain in less than three hours, and 16% (n=45) had no pain after one hour (Weber et al, 2003).
* 1) None of the patients required fibrinolytic agents and only 4 patients received a beta antagonist. Congestive heart failure or dysrhythmias were not reported. After 9 hours of observation, a cardiology consult was obtained, with 158 of the 302 patients undergoing stress testing before discharge. Only 4 patients tested positive and underwent cardiac catherization. Thirty day survival was obtained in 300 patients with no deaths related to cardiovascular events; four patients who continued cocaine use after discharge did develop nonfatal myocardial infarctions.
* 2) The authors concluded that patients with cocaine-associated chest pain can be safely evaluated, treated and discharged to home after a 9 to 12 hour observation period. However, patients with recurrent symptoms, ECG or laboratory evidence of myocardial ischemia, or dysrhythmias require further evaluation and treatment.

* 6.4 MONITORING
o A) Blood or plasma cocaine levels are not clinically useful, although they may be helpful in selected forensic cases.
o B) Qualitative urine confirmation may assist in diagnosis.
o C) An ECG is indicated in all patients.
o D) CBC, electrolytes, urinalysis, and CPK or troponin levels may be indicated in moderate to severe poisoning cases.
o E) Radiologic evaluation may be of value in evaluating body packers.

* 6.5 ORAL EXPOSURE
o 6.5.2 PREVENTION OF ABSORPTION
+ A) SUMMARY
-- 1) As most cocaine exposures are through the intranasal, intravenous, or intrapulmonary (smoking) routes, attempts at preventing absorption are not generally useful (Schwartz & Oderda, 1980).
* a) In cases where a recent large oral ingestion of cocaine powder is suspected, attempts to empty the stomach are warranted.
* b) If the patient is comatose, seizing, or without a gag reflex the patient's airway should be protected with a cuffed endotracheal tube and gastric lavage done, followed by instillation of 60 to 100 grams of activated charcoal.
* c) IN VITRO ADSORPTION - Activated charcoal adsorbs cocaine in vitro under both acidic and alkaline conditions (Tomaszewski et al, 1992).

+ B) ACTIVATED CHARCOAL
-- 1) CHARCOAL ADMINISTRATION
* a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka & Seger, 1997). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.

-- 2) CHARCOAL DOSE
* a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 1 gram/kilogram in infants up to 1 year old (USP DI, 2002)(Chyka & Seger, 1997).
o 1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (Barceloux et al, 1997).

* b) ADVERSE EFFECTS/CONTRAINDICATIONS
o 1) Complications: emesis, aspiration (Chyka & Seger, 1997). Aspiration may be complicated by acute respiratory failure, ARDS or bronchiolitis obliterans (Pollack et al, 1981; Harris & Filandrinos, 1993; (Elliot et al, 1989) Harsh, 1986; (Rau et al, 1988)(Golej et al, 2001)(Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
o 2) Contraindications: unprotected airway, gastrointestinal tract not anatomically intact, therapy may increase the risk or severity of aspiration; ingestion of most hydrocarbons (Chyka & Seger, 1997).

o 6.5.3 TREATMENT
+ A) SUPPORTIVE CARE
-- 1) For most "mild" intoxications involving sinus tachycardia and mildly elevated blood pressure, supportive care is the treatment of choice (Orr & Jones, 1968).

+ B) SEIZURE
-- 1) SUMMARY
* a) Attempt initial control with a benzodiazepine (diazepam or lorazepam). If seizures persist or recur administer phenobarbital.
* b) Monitor for respiratory depression, hypotension, dysrhythmias, and the need for endotracheal intubation.
* c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or treat with intravenous dextrose ADULT: 50 milliliters IV, CHILD: 2 milliliters/kilogram 25% dextrose).

-- 2) DIAZEPAM
* a) MAXIMUM RATE: Administer diazepam intravenously over 2 to 3 minutes (maximum rate = 5 milligrams/minute).
* b) ADULT DIAZEPAM DOSE: 5 to 10 milligrams initially, repeat every 5 to 10 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 30 milligrams.
* c) PEDIATRIC DIAZEPAM DOSE: 0.2 to 0.5 milligram per kilogram repeat every 5 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 10 milligrams in children over 5 years or 5 milligrams in children under 5 years of age.
* d) RECTAL USE: If an intravenous line cannot be established, diazepam may be given per rectum (generally use twice the usual initial dose because of decreased absorption). Rectal formulations are available in fixed, unit doses of 5, 10, 15 and 20 mg (Prod Info Diastat(R) Diazepam gel in a rectal delivery system, 1999). Recommended dose is 0.2 to 0.5 mg/kg depending on age. Lorazepam may also be given intramuscularly.
* e) MIDAZOLAM: has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. PEDIATRIC MIDAZOLAM DOSE: INTRAMUSCULAR: 0.2 milligram/kilogram (maximum 7 milligrams) (Chamberlain et al, 1997); INTRANASAL: 0.2 milligram/kilogram (Lahat et al, 2000). Buccal midazolam, 10 milligrams, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

-- 3) LORAZEPAM
* a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 milligrams/minute (Prod Info Ativan(R), 1999).
* b) ADULT LORAZEPAM DOSE: 2 to 4 milligrams intravenously. Initial doses may be repeated in 10 to 15 minutes if seizures persist (Prod Info, Ativan(R), 1999; AMA, 1991).
* c) PEDIATRIC LORAZEPAM DOSE: 0.05 to 0.1 milligram/kilogram intravenously, (maximum 4 milligrams/dose) repeated twice at intervals of 10 to 15 minutes (Benitz & Tatro, 1995).

-- 4) PHENOBARBITAL
* a) ADULT PHENOBARBITAL LOADING DOSE: 600 to 1200 milligrams of phenobarbital intravenously initially (10 to 20 milligrams per kilogram) diluted in 60 milliliters of 0.9 percent saline given at 25 to 50 milligrams per minute.
* b) ADULT PHENOBARBITAL MAINTENANCE DOSE: Additional doses of 120 to 240 milligrams may be given every 20 minutes.
* c) MAXIMUM SAFE ADULT PHENOBARBITAL DOSE: No maximum safe dose has been established. Patients in status epilepticus have received as much as 100 milligrams/minute until seizure control was achieved.
* d) PEDIATRIC PHENOBARBITAL LOADING DOSE: 15 to 20 milligrams per kilogram of phenobarbital intravenously at a rate of 25 to 50 milligrams per minute.
* e) PEDIATRIC PHENOBARBITAL MAINTENANCE DOSE: Repeat doses of 5 to 10 milligrams per kilogram may be given every 20 minutes.
* f) MAXIMUM SAFE PEDIATRIC PHENOBARBITAL DOSE: No maximum safe dose has been established. Children in status epilepticus have received doses of 30 to 120 milligrams/kilogram within 24 hours. Vasopressors and mechanical ventilation were needed in some patients receiving these doses.
* g) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation.
* h) NEONATAL PHENOBARBITAL LOADING DOSE: 20 to 30 milligrams/kilogram intravenously at a rate of no more than 1 milligram/kilogram per minute in patients with no preexisting phenobarbital serum levels.
* i) NEONATAL PHENOBARBITAL MAINTENANCE DOSE: Repeat doses of 2.5 milligrams/kilogram every 12 hours may be given; adjust dosage to maintain serum levels of 20 to 40 micrograms/milliliter.
* j) MAXIMUM SAFE NEONATAL PHENOBARBITAL DOSE: Doses of up to 20 milligrams/kilogram/minute up to a total of 30 milligrams/kilogram have been tolerated in neonates.
* k) CAUTIONS: Adequacy of ventilation must be continuously monitored in children and adults. Intubation may be necessary with increased doses.
* l) SERUM LEVEL MONITORING: Monitor serum levels over next 12 to 24 hours for maintenance of therapeutic levels (20 to 40 micrograms per milliliter).

-- 5) ANIMAL STUDY - In a rat model, pretreatment with diazepam did not prevent cocaine induced death from etiologies other than seizures. The incidence of death was reduced if prazosin was used with diazepam prior to cocaine intoxication (Tseng et al, 1993).
-- 6) ANIMAL STUDY - In a study of newly approved antiepileptic drugs in a murine model, treatment with agents that enhance GABA-mediated neuronal inhibition, especially gabapentin, offered better protection against cocaine-induced seizures compared to agents with sodium and calcium channel blockade as a primary mechanism of action (Gasior et al, 1999).

+ C) GRAND MAL STATUS
-- 1) RECURRING SEIZURES
* a) If seizures are not controlled by the above measures, consider continuous infusions of MIDAZOLAM (LOADING DOSE: 0.2 milligram/kilogram slow bolus, INFUSION: 0.75 to 10 micrograms/kilogram/minute), PROPOFOL (INITIAL: 1 to 2 milligrams/kilogram, MAINTENANCE: 2 to 10 milligrams/kilogram/hour) or PENTOBARBITAL (LOADING DOSE: 10 to 15 milligrams/kilogram at a rate of 50 milligrams/minute until burst suppression or electrocerebral inactivity on EEG; MAINTENANCE: 0.5 to 1 milligram/kilogram/hour) (Anon, 1993).
* b) Endotracheal intubation, mechanical ventilation, and vasopressors will be required and consultation with a neurologist is strongly advised.
* c) Neuromuscular paralysis may be required to avoid hyperthermia, severe acidosis, and rhabdomyolysis; continuous EEG monitoring is mandatory if neuromuscular paralysis is used.

+ D) HYPOTENSIVE EPISODE
-- 1) Because chronic cocaine abuse results in depletion of norepinephrine, an indirect vaso pressor, such as dopamine, would be theoretically less effective than a direct agonist, such as norepinephrine.
-- 2) NOREPINEPHRINE
* a) PREPARATION: Add one milligram norepinephrine to 250 milliliters of dextrose 5% in water to produce 4 micrograms/milliliter.
* b) DOSE
o 1) ADULT: begin infusion at 0.5 to 1 microgram/minute and titrate to maintain adequate blood pressure (AHA, 2000).
o 2) CHILD: begin infusion at 0.1 microgram/kilogram/minute and titrate to maintain adequate blood pressure.
o 3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised.

-- 3) DOPAMINE
* a) PREPARATION: Add 400 milligrams to 250 milliliters of normal saline or dextrose 5% in water to produce 1600 micrograms per milliliter or add 400 milligrams to 500 milliliters of normal saline or dextrose 5% in water to produce 800 micrograms per milliliter.
* b) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed. Norepinephrine should be added if more than 20 micrograms/kilogram/minute of dopamine is needed.
* c) CAUTION: If VENTRICULAR DYSRHYTHMIAS occur, decrease rate of administration. Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred.

+ E) HYPERTENSIVE EPISODE
-- 1) Little morbidity or mortality has been attributable to cocaine-induced hypertension (Schwartz & Oderda, 1980)(Goldfrank et al, 1981)(Bettinger, 1980)(Gilman et al, 1980). Hypertension is usually short-lived and often followed by significant hypotension. Mild hypertension generally responds to sedation with benzodiazepines.
-- 2) Monitor vital signs regularly. For mild/moderate asymptomatic hypertension, pharmacologic intervention is generally not necessary. Sedative agents such as benzodiazepines may be helpful in treating hypertension and tachycardia in agitated patients, especially if a sympathomimetic agent is involved in the poisoning.
-- 3) For hypertensive emergencies (severe hypertension with evidence of end organ injury (CNS, cardiac, renal), or emergent need to lower mean arterial pressure 20% to 25% within one hour), nitroprusside is preferred. Nitroglycerin and phentolamine are possible alternatives. * TREATMENT
o ORAL EXPOSURE
+ TREATMENT
-- HYPERTENSIVE EPISODE
* 4) HYPERTENSIVE EMERGENCY
o a) CASE REPORT - Acute hypertension was associated with aortic dissection in one case (Grannis et al, 1988).
o b) NITROPRUSSIDE/INDICATIONS
+ 1) Preferred for emergent treatment of severe hypertension secondary to poisonings. Short duration of action allows accurate titration of blood pressure, as the hypertensive effects of drug overdoses are often short lived (AHA, 2000).
o c) NITROPRUSSIDE/DOSE
+ 1) Begin intravenous infusion at 0.1 microgram/kilogram/minute and titrate to desired effect; up to 10 micrograms/kilogram/minute may be required (AHA, 2000). Frequent hemodynamic monitoring and administration by an infusion system that ensures a precise flow rate is mandatory.
o d) NITROPRUSSIDE/SOLUTION PREPARATION
+ 1) Dilute a 50-milligram vial in 500 milliliters of dextrose 5 percent in water (100 micrograms/milliliter). Prepare fresh every 24 hours; wrap in aluminum foil. Discard discolored solution.
o e) NITROPRUSSIDE/MAJOR ADVERSE REACTIONS
+ 1) Severe hypotension; headaches, nausea, vomiting, abdominal cramps; thiocyanate or cyanide toxicity; methemoglobinemia; lactic acidosis; chest pain or dysrhythmias (high doses). The addition of 1 gram of sodium thiosulfate to each 100 milligrams of sodium nitroprusside for infusion may help to prevent cyanide toxicity in patients receiving prolonged or high dose infusions.
o f) NITROPRUSSIDE/MONITORING PARAMETERS
+ 1) Monitor blood pressure every 30 to 60 seconds at onset of drip; once stabilized, monitor every 5 minutes.
o g) NITROGLYCERIN/INDICATIONS
+ 1) May be used in addition to nitroprusside to control hypertension (particularly useful in patients with coronary artery disease or congestive heart failure).
o h) NITROGLYCERIN/ADULT DOSE
+ 1) Begin infusion at 10 to 20 micrograms/minute and increase by 5 or 10 micrograms/minute every 5 to 10 minutes until the desired hemodynamic response is achieved (AHA, 2000).
o i) NITROGLYCERIN/PEDIATRIC DOSE
+ 1) 1 microgram/kilogram/minute by continuous infusion; increase by 1 microgram/kilogram/minute every 20 to 60 minutes as needed until the desired hemodynamic response is achieved (Benitz & Tatro, 1995a).
o j) PHENTOLAMINE/INDICATIONS
+ 1) Useful for severe hypertension caused by agents with alpha adrenergic agonist effects. Generally reserved for cases not responsive to shorter acting, titratable agents, such as nitroprusside.
o k) PHENTOLAMINE/ADULT DOSE
+ 1) Administer 5 milligrams doses intravenously repeated as needed until hypertension is controlled (USP DI, 2002).
o l) PHENTOLAMINE/PEDIATRIC DOSE
+ 1) 0.05 to 0.1 milligram/kilogram (2.5 milligrams maximum) intravenously every 5 minutes until hypertension is controlled, then every 2 to 4 hours as needed (Benitz & Tatro, 1995a).
o m) PHENTOLAMINE/ADVERSE EFFECTS
+ 1) Hypotension, dysrhythmias, angina, tachycardia, nausea, vomiting, abdominal pain, diarrhea.
* 5) BETA ADRENERGIC BLOCKERS
o a) If severe hypertension and/or hemodynamically significant tachycardia do not respond to sedation with benzodiazepines, beta adrenergic blocking agents may be of benefit. A short acting, cardioselective agent such as esmolol is generally preferred. Paradoxical worsening from unopposed alpha agonist effects is a theoretical possibility.
o b) PROPRANOLOL - The use of propranolol to specifically treat cocaine-induced hypertension may result in "paradoxical hypertension" (Ramoska & Sacchetti, 1985). Unopposed alpha stimulation was suggested as the cause.
+ 1) ANIMAL STUDY - Propranolol blocked cocaine-induced cerebral vasodilation and decreased the acute hypertensive response in newborn sheep. The authors suggested that beta receptors played a role in the actions of cocaine on the cerebrovascular system (O'Brien et al, 1999). A blunted increase in mean arterial pressure with no change in catecholamine levels was seen in the sheep following propranolol therapy.
+ 2) Leikin (1999) suggested a reappraisal of the value of beta antagonists in the treatment of hyperadrenergic effects associated with cocaine toxicity. Beta antagonists may be valuable for treatment of peripheral cardiovascular pressor effects.
+ 3) ANIMAL STUDY - An animal study suggests that cocaine-induced cardiotoxicity is likely due to peripheral effects of cocaine on the cardiovascular system rather than centrally-mediated increased sympathetic outflow (Dickerson et al, 1999).
o c) LABETALOL, which has both alpha and beta blocking properties, may be preferable to propranolol (Dusenberry et al, 1987)(Bessen, 1987). Labetalol infusion was used successfully in a patient with cocaine-induced hypertensive crisis following ingestion of 20 grams of cocaine (14 grams retrieved by lavage) (Gay & Loper, 1988).
+ 1) However, paradoxical hypertension has also been seen in patients receiving labetalol for the treatment of pheochromocytoma-induced hypertension (Reach, 1980) Briggs et al, 1988; (Bessen, 1987).
+ 2) Labetalol reduced mean arterial pressure but did not reverse cocaine-induced coronary artery constriction in human volunteers (Boehrer et al, 1993).
o d) LABETALOL/INTRAVENOUS INDICATIONS
+ 1) Consider if severe hypertension is unresponsive to short acting titratable agents such as nitroprusside. Use cautiously if sympathomimetic agents are involved in the poisoning, as worsening hypertension may develop from alpha adrenergic effects despite the mixed alpha and beta adrenergic effects of labetalol.
o e) LABETALOL/ADULT DOSE
+ 1) INTRAVENOUS BOLUS: Initial dose of 20 milligrams by slow injection over 2 minutes. Repeat with 40 to 80 milligrams every 10 to 15 minutes. Maximum total dose 300 milligrams. Maximum effects on blood pressure usually occur in 5 minutes (Prod Info, Normodyne(R), 1999).
+ 2) INTRAVENOUS INFUSION: Add 200 milligrams labetalol to 160 milliliters of intravenous fluid to create a solution containing 1 milligram/milliliter. Administer infusion after initial bolus as above until desired blood pressure is reached (Prod Info Normodyne(R), labetalol, 1999). Use of an infusion pump is recommended.
o f) LABETALOL/PEDIATRIC DOSE
+ 1) INTRAVENOUS: LOADING DOSE: 0.2 to 1 milligram/kilogram. INFUSION: 0.25 to 1.5 milligram/kilogram/hour (Benitz & Tatro, 1995a).
o g) LABETALOL/DOSING IN SPECIAL SITUATIONS
+ 1) Reduce dose in hepatic insufficiency; dose reduction not required in renal failure.
o h) LABETALOL/ADVERSE REACTIONS
+ 1) Postural hypotension causing dizziness; fatigue; tremors; abdominal cramps.
+ 2) MAJOR ADVERSE REACTIONS: Withdrawal reactions observed mainly in patients who have received large doses (more than 1.2 milligrams daily, or those who are also receiving a beta- blocker).
+ 3) Decrease dose gradually over a period of one week or more; if withdrawn prior to emergency, control blood pressure with sodium nitroprusside, either alone or in combination with phentolamine.
o i) LABETALOL/PRECAUTIONS
+ 1) Contraindicated in patients with pheochromocytoma, bronchial asthma, congestive heart failure, greater than first degree heart block, cardiogenic shock, or severe bradycardia (Med Lett, 1989)(Wright et al, 1986).
+ 2) Use caution in hepatic disease or intermittent claudication; effects of halothane may be enhanced by labetalol; safe for use in pregnancy.
o j) LABETALOL/MONITORING PARAMETERS: Monitor blood pressure frequently during initial dosing and infusion.
* F) VENTRICULAR ARRHYTHMIA
o 1) VENTRICULAR DYSRHYTHMIAS SUMMARY
+ a) Obtain an ECG, institute continuous cardiac monitoring and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders (particularly hypokalemia, hypocalcemia, and hypomagnesemia). Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Sotalol is an alternative for stable monomorphic ventricular tachycardia. Amiodarone and sotalol should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require cardioversion. Atropine may be used when severe bradycardia is present and PVCs are thought to represent an escape complex.
o 2) LIDOCAINE
+ a) LIDOCAINE/INDICATIONS
-- 1) Ventricular tachycardia or ventricular fibrillation. Consider in patients with frequent PVCs (greater than 5 per minute), coupled, multifocal, or R on T phenomenon associated with ingestion.
+ b) LIDOCAINE/DOSE
-- 1) ADULT: 1 to 1.5 milligram/kilogram intravenously push. For refractory VT/VF an additional bolus of 0.5 to 0.75 milligram/kilogram can be given over 3 to 5 minutes. Total dose should not exceed 3 milligrams/kilogram or more than 200 to 300 milligrams during a one hour period (AHA, 2000). Only bolus therapy is recommended during cardiac arrest.
* a) Once circulation has been restored begin maintenance infusion of 1 to 4 milligrams per minute. If dysrhythmias recur during infusion repeat 0.5 milligram/kilogram bolus an increase the infusion rate incrementally (maximal infusion rate is 4 milligrams/minute) (AHA, 2000).
-- 2) CHILD: 1 milligram/kilogram initial bolus intravenously; followed by a continuous infusion of 20 to 50 micrograms/kilogram/minute (AHA, 2000).
+ c) LIDOCAINE/PREPARATION
-- 1) Add 1 gram of lidocaine to 250 milliliters of dextrose 5 percent in water, to make a 4 milligram/milliliter solution. An increase in the infusion rate of 1 milliliter/minute increases the dose by 4 milligrams/minute.
+ d) LIDOCAINE/DOSING IN SPECIAL SITUATIONS
-- 1) Although the loading dose of lidocaine does not need to be reduced, the maintenance dose should be decreased by 50% in the presence of decreased cardiac output (hypotension or shock, congestive heart failure, poor peripheral perfusion) and in patients over 70 years of age and those with hepatic dysfunction (AHA, 2000).
+ e) LIDOCAINE/MAJOR ADVERSE REACTIONS
-- 1) Paresthesias; muscle twitching; confusion; slurred speech; seizures; respiratory depression or arrest; bradycardia; coma. May cause significant AV block or worsen pre-existing block. Prophylactic pacemaker may be required in the face of bifascicular, second degree, or third degree heart block.
+ f) LIDOCAINE/MONITORING PARAMETERS
-- 1) ECG; plasma concentrations.
+ g) CAUTIONS - Because lidocaine is a local anesthetic agent as is cocaine, it may theoretically not the antiarrhythmic of choice for cocaine-induced ventricular arrhythmias.
+ h) In a retrospective study of 155 patients with cocaine associated myocardial infarction, medical records were available for 26 of 29 patients who received lidocaine (Shih et al, 1994). One patient developed confusion which may have been related to the lidocaine; no other adverse effects were recorded.
+ i) ANIMAL DATA
-- 1) In one rat study, lidocaine potentiated cocaine induced seizures and death (Derlet et al, 1991).
-- 2) Lidocaine, used either as a pretreatment or therapy, did not increase the duration of seizures in cocaine intoxicated swine (McKinney et al, 1993)(McKinney et al, 1992).
o 3) AMIODARONE
+ a) AMIODARONE/INDICATIONS
-- 1) Effective for the control of hemodynamically stable ventricular tachycardia, polymorphic ventricular tachycardia, and wide complex tachycardia of unclear origin. Also recommended after defibrillation and epinephrine in cardiac arrest with persistent ventricular tachycardia or ventricular fibrillation (AHA, 2000). It should be used with caution when the ingestion involves agents with quinidine-like effects (e.g. tricyclic antidepressants, phenothiazines, chloroquine, antidysrhythmics) and when the ECG reveals QRS widening or QT prolongation suspected to be secondary to overdose.
+ b) AMIODARONE/ADULT DOSE
-- 1) Infuse 150 milligrams over 10 minutes, followed by a 1 milligram/minute infusion for 6 hours then 0.5 milligram/minute. Subsequent infusion of 150 milligrams can be repeated as needed for recurrent or resistant dysrhythmias to a maximum total daily dose of 2 grams (AHA, 2000).
+ c) AMIODARONE/PEDIATRIC DOSE
-- 1) Infuse 5 milligrams/kilogram as a bolus for pulseless ventricular tachycardia or ventricular fibrillation. Infuse 5 milligrams/kilogram over 20 to 60 minutes for perfusing tachycardias. Maximum total dose is 15 milligrams/kilogram per day. Routine use with other drugs that prolong the QT interval is NOT recommended.
+ d) ADVERSE EFFECTS
-- 1) Hypotension and bradycardia are the most common adverse effects. Treat by slowing infusion, intravenous crystalloid administration, pressors or pacing (AHA, 2000).
o 4) BETA ADRENERGIC BLOCKERS
+ a) Beta adrenergic blocking agents should be avoided in patients with cocaine associated myocardial ischemia or infarction. This class of drugs has been shown to potentiate coronary vasoconstriction (Lange et al, 1990).
+ b) NOTE - Propranolol is NOT a SPECIFIC antidote for cocaine overdose. Propranolol has been associated with increased blood pressure in the setting of cocaine overdose, presumably due to unopposed alpha adrenergic stimulation (Ramoska & Sacchetti, 1985). Beta blockers have demonstrated poor clinical efficacy in several studies (Trouve et al, 1985).
o 5) LABETALOL may be preferable in hypertensive patients due to its alpha and beta blocking properties (Dusenberry et al, 1987)(Gay & Loper, 1988).
+ a) RECOMMENDED DOSE - 0.25 milligram/kilogram by slow intravenous injection over 2 minutes. Titrate to clinical response. Patients should be supine, have continuous cardiac monitoring, and blood pressure should be checked every few minutes.
o 6) CALCIUM CHANNEL BLOCKERS
+ a) In a human study of isradipine treatment on the effects of cocaine use, isradipine did not attenuate cocaine-induced increase in blood pressure in six otherwise healthy subjects (Johnson et al, 1999).
-- 1) Experimental animal studies of calcium channel blockers in cocaine toxicity have had mixed results. Calcium channel blockers suppressed cocaine-induced arrhythmias, vasoconstriction, and myocardial depression but may increase the incidence of seizures. Influence on survival has been variable.
-- 2) Diltiazem, flunarizine, nifedipine, and verapamil completely suppressed cocaine-induced ventricular fibrillation in cocaine intoxicated dogs (Billman, 1993).
-- 3) Nitrendipine protected against cocaine toxicity (increased survival time and lethal dose) in two experimental animal studies (Nahas et al, 1985)(Trouve et al, 1985).
-- 4) Nitrendipine offered slight protection from the functional depressant effects of higher concentrations of cocaine on rat myocardial cell cultures, but it did not prevent cocaine induced membrane damage or morphological alterations (Melchert et al, 1991).
-- 5) In rats, nitrendipine pretreatment inhibited arteriolar vasoconstriction induced by cocaine (Vicaut et al, 1991).
-- 6) In rats, pretreatment with diltiazem, nifedipine, and verapamil potentiated cocaine induced seizures and lethality (Derlet & Albertson, 1989).
o 7) ESMOLOL
+ a) No consistent hemodynamic benefit has been found with this drug. Hypertension, hypotension, and lethargy requiring endotracheal intubation have been reported (Sand et al, 1991).
+ b) May be useful for rapid control of sinus tachycardia or supraventricular tachycardia due to its beta-1 selectivity and its short duration of action (half-life: 0.15 hour) (Olin, 1990).
+ c) DOSE - Administer a loading dose of 500 micrograms/kilogram/minute for one minute, followed by a maintenance infusion of 50 to 200 micrograms/kilogram/minute (Olin, 1990).
+ d) Pollan & Tadjziechy (1989) reported the successful use of esmolol infusion to treat tachycardia and hypertension due to cocaine.
o Cool

SODIUM BICARBONATE
+ a) Sodium bicarbonate may be useful in the treatment of QRS widening and ventricular dysrhythmias associated with acute cocaine use. A reasonable starting dose is 1 to 2 mEq/kg repeated as needed. Monitor arterial blood gases, target pH 7.45 to 7.55.
+ b) In one animal study, it was shown that sodium bicarbonate reverses the dose-dependent slowing of cardiac conduction produced by cocaine. The lack of efficacy of sodium chloride suggests that this reversal is mediated by alkalosis rather than by an increase in extracellular sodium concentration (Parker et al, 1999).
+ c) EXPERIMENTAL ANIMALS - Sodium bicarbonate decreased cocaine-induced QRS prolongation to nearly baseline in anesthetized dogs (Beckman et al, 1991).
-- 1) In another study, cocaine-induced conduction abnormalities and resultant hemodynamic compromise were observed in mongrel dogs given three successive doses of cocaine (7 mg/kg) (the doses given were an attempt to be similar to a "recreational" dose that might be used in an individual) in 15 anesthetized dogs. After NaHCO(3) was administered to the treatment group (n=5; two dogs died of dysrhythmias prior to treatment), the QRS duration immediately decreased by 30% and returned to baseline more quickly than the placebo group, cardiac output (measured 3 minutes after administration) improved by 78% (95% CI) and remained significantly increased throughout the observation period. The authors concluded that NaHCO(3) improved ECG changes secondary to cocaine toxicity and improved myocardial function (Wilson & Shelat, 2003).
* G) ACIDOSIS
o 1) Correction of acidemia through supportive care measures such as hyperventilation, sedation, active cooling, and sodium bicarbonate infusion resulted in improvement of conduction defects in a case series of 4 patients (Wang, 1999).
* H) BODY TEMPERATURE ABOVE NORMAL
o 1) Hyperthermia is frequently associated with a fatal outcome (Catravas & Waters, 1981) and should be treated aggressively if severe.
+ a) Place patient in a cool room.
+ b) Minimize physical activity and sedate with benzodiazepines (large doses may be necessary). Sponge patient with tepid to cool water and use fans to maximize evaporative heat loss.
+ c) Place patient on a hypothermia blanket.
o 2) Other cooling methods include convection evaporation, intubation and cool air ventilation, and gastric lavage with iced saline (Bauwens et al, 1989).
o 3) CHLORPROMAZINE - AVOID in cocaine overdose because it may lower the seizure threshold.
o 4) HALOPERIDOL - Associated with increased incidence of dystonic reactions among cocaine abusers (Kumor et al, 1986).
o 5) Refractory cases may require sedation and neuromuscular paralysis.
* I) FEELING AGITATED
o 1) Agitated patients are best treated in a calm, reassuring manner. Place patient in a dark, quiet area if possible.
o 2) Hypoglycemia may cause agitation and mimic acute cocaine intoxication. Consider as a differential diagnosis in patients presenting with mental status changes; obtain blood glucose level and administer intravenous dextrose solution if necessary (Brady & Duncan, 1999).
o 3) Intravenous DIAZEPAM (Adults: 5 to 10 milligrams every 5 to 10 minutes as needed; Child: 0.1 to 0.2 milligram/kilogram every 5 to 10 minutes as needed) may be helpful (Anon, 1984). Large doses may be necessary in severe cases. Monitor for respiratory depression and need for endotracheal intubation.
o 4) CHLORPROMAZINE - CAUTIONS - has been used for amphetamine psychosis, but when given intravenously may cause hypotension, and lower seizure threshold.
o 5) Lithium has been used in the management of acute cocaine induced psychosis (hallucinations, paranoia, grandiosity, and hyperactivity) but further clinical studies are needed to substantiate these findings (Scott & Mullaly, 1981).
* J) DRUG WITHDRAWAL
o 1) SUMMARY - A cocaine withdrawal syndrome including depression, irritability, sleep disturbances, GI symptoms, and headache has been described (Schnoll et al, 1984), with onset 24 to 48 hours after drug use is discontinued and lasting 7 to 10 days. Cocaine dependency and withdrawal is a complex medical and psychosocial problem with no known effective treatment (Kleber & Gawin, 1984).
o 2) BROMOCRIPTINE has successfully reduced cocaine craving and decreased withdrawal symptoms in several studies (Dackis et al, 1987)(Giannini et al, 1987) Tennant & Sagherain, 1987).
o 3) BUPRENORPHINE has been used to treat cocaine addiction; it should be used with caution, as it is also addictive (Stimmel, 1991).
o 4) CARBAMAZEPINE was successful in increasing length of cocaine abstinence in one study (Halikas et al, 1991).
o 5) ANTIDEPRESSANTS - Tricyclic antidepressants (specifically desipramine, imipramine, and maprotiline), bupropion, lithium, and methylphenidate have been used to treat cocaine withdrawal with mixed success (Kleber & Gawin, 1984)(Lacombe et al, 1991)(Margolin et al, 1991).
o 6) AMANTADINE - Kampman et al (2000) suggested that amantadine may be an effective treatment for cocaine-dependent patients with severe cocaine withdrawal symptoms.
o 7) DISULFIRAM - Petrakis et al (2000) reported that disulfiram may be an effective treatment for cocaine dependence in methadone-maintained opioid addicts, even in those individuals without co-morbid alcohol abuse. It was suggested that disulfiram inhibits dopamine beta-hydroxylase resulting in an excess of dopamine and decreased synthesis of norepinephrine. Since cocaine is a potent catecholamine reuptake inhibitor, disulfiram may reduce cocaine craving or alter the "high".
* K) CHEST PAIN
o 1) NITROGLYCERIN
+ a) Nitroglycerin appears to be safe and may be effective in treating cocaine associated chest pain (Hollander et al, 1994). In a study of cocaine related chest pain, 37 of 83 patients receiving nitroglycerin had relief of pain, 2 had resolution of ischemic changes on ECG, 2 had control of hypertension, and 1 had improvement of CHF (Hollander et al, 1994).
+ b) One patient who sustained an inferior myocardial infarction with right ventricular involvement developed transient hypotension after nitroglycerin administration.
+ c) Sublingual nitroglycerin, in a dose sufficient to reduce mean systemic arterial pressure by 10 to 15 percent, alleviates cocaine-induced vasoconstriction in diseased and nondiseased coronary arteries (Brogan et al, 1991).
+ d) In one study, the concurrent use of diazepam and nitroglycerin for treatment of patients with potential cocaine-associated acute coronary syndrome did not offer any additional benefit over either agent alone (Baumann et al, 2000a).
+ e) In a prospective, randomized trial of benzodiazepines and nitroglycerin (NTG) use as compared to nitroglycerin alone for the treatment of cocaine-induced acute coronary syndrome, nitroglycerin with lorazepam was more efficacious in relieving chest pain than nitroglycerin alone. The study consisted of 36 patients with the average age being 34.1 years with 67% being men. Exclusion criteria included age greater than 45 years, documented coronary artery disease or pretreatment with nitroglycerin, or chest pain of more than 72 hours (Honderick et al, 2003).
+ f) Group 1 consisted of 15 patients who received 0.4 mg NTG sublingually initially, followed by another dose as needed in 5 minutes if chest pain persisted. Group 2 had 12 patients that received 0.4 mg sublingual NTG and a 1 milligram intravenous bolus of lorazepam initially, followed by repeat doses of both medications 5 minutes later if chest pain persisted. All patients received oxygen and 325 mg aspirin. Pain measurement was scored with a self-reported numeric pain scale of 0 to 10. Baseline pain scores were 6.87 for group 1 and 6.54 for group 2; five minutes after initial treatment the mean scores were 5.20 and 3.96, respectively with a difference of 1.24 (95% CI -0.080 to 3.29). After an additional 5 minutes, the scores were 4.60 for group 1 and 1.50 for group 2, with a difference in means of 3.10 (95% CI 1.22 to 4.9 Cool

. No patient in either group met the criteria for an acute MI or had cardiac complications. Limitations included: self reported cocaine use with limited or no laboratory confirmation. Further study is recommended.
o 2) THROMBOLYTICS
+ a) In a retrospective study of 155 patients with cocaine associated myocardial infarction, 23 patients received thrombolytics (Hollander et al, 1994). No major complications or deaths occurred, 1 patient developed a febrile reaction to streptokinase and 1 developed vaginal bleeding not requiring transfusion.
+ b) In several studies, cautions about the use of thrombolytics in cocaine-associated acute myocardial infarction (AMI) have been made. These studies have suggested that because AMI mortality may be low in young patients with cocaine use, the risks outweigh the benefits of thrombolytic therapy. Other studies reported that these cautions would require unnecessary toxicology screening before treatment of patients with AMI who deny cocaine use, and unnecessarily delay treatment of patients with AMI who admit to cocaine use (Boniface & Feldman, 2000).COCAINE

* TREATMENT
o ORAL EXPOSURE
+ TREATMENT
-- CHEST PAIN
* c) Thrombolytics should be avoided in patients with cocaine induced myocardial infarction and uncontrolled hypertension, because of the increased risk of intracranial hemorrhage.
o 3) PHENTOLAMINE
+ a) EXPERIMENTAL USE - Cocaine-induced coronary vasoconstriction and myocardial ischemia can be reversed by the intracoronary administration of phentolamine (Lange et al, 1989).
+ b) CASE REPORT - Intravenous phentolamine (1 milligram) relieved cocaine-induced chest pain in one case report (Hollander et al, 1992a).
o 4) DOBUTAMINE
+ a) In a pilot study, to evaluate the safety of dobutamine stress echocardiography (DSE) in emergency department patients with cocaine-associated chest pain, none of the patients experienced exaggerated adrenergic response (Dribben et al, 2001).
o 5) TIROFIBAN
+ a) In one case report, tirofiban, an antiplatelet agent which binds to the platelet receptor glycoprotein IIb/IIIa and inhibits platelet aggregation, was successfully used to treat cocaine-induced coronary artery thrombosis (Frangogiannis et al, 1999).
* L) RHABDOMYOLYSIS
o 1) SUMMARY: Early aggressive fluid replacement is the mainstay of therapy and may help prevent renal insufficiency. Diuretics such as mannitol or furosemide may be needed to maintain urine output. Urinary alkalinization is NOT routinely recommended.
o 2) Initial treatment should be directed towards controlling acute metabolic disturbances such as hyperkalemia, hyperthermia, and hypovolemia. Control seizures, agitation, and muscle contractions.
o 3) Vigorous fluid replacement with 0.9% saline is necessary even if there is no evidence of dehydration. Hypovolemia, increased insensible losses, and third spacing of fluid commonly increase fluid requirements. Strive to maintain a urine output of at least 2 to 3 milliliters/kilogram per hour. In severe cases 500 milliliters of fluid per hour may be required for the first several days. Monitor fluid input and urine output, plus insensible losses. Monitor for evidence of fluid overload and compartment syndrome; monitor serum electrolytes, CK, and renal function tests.
o 4) Alkalinization of the urine is not routinely recommended as it has never been documented to reduce nephrotoxicity and may cause complications such as alkalemia, hypocalcemia, and hypokalemia.
* M) EXPERIMENTAL THERAPY
o 1) EXPERIMENTAL ANIMAL STUDIES - Magnesium pretreatment reduced cocaine lethality in rats (Mouton et al, 1992).
o 2) ANIMAL STUDIES - In mice, N-methyl-D-aspartate (NMDA) antagonists reduced cocaine-induced seizures in a dose-dependent fashion. The NMDA antagonists were also more efficacious than traditional anticonvulsant agents, such as diazepam and phenobarbital, in the mouse model (Witkin et al, 1999).
* N) SEROTONIN SYNDROME
o 1) HYPERTHERMIA
+ a) Control agitation and muscle activity. Undress patient and enhance evaporative heat loss by keeping skin damp and using cooling fans.
+ b) MUSCLE ACTIVITY - Benzodiazepines may be useful. Diazepam: Adult: 5 to 10 milligrams IV every 5 to 10 minutes as needed, monitor for respiratory depression and need for intubation. Child: 0.25 milligram/kilogram IV every 5 to 10 minutes; monitor for respiratory depression and need for intubation.
+ c) Non-depolarizing paralytics may be used in severe cases.
o 2) HYPERTENSION
+ a) Monitor vital signs regularly. For mild/moderate asymptomatic hypertension, pharmacologic intervention is usually not necessary. For hypertensive emergencies (emergent need to lower mean BP 30 percent within 30 minutes and achieve diastolic BP of 100 mmHg or less within one hour), nitroprusside is preferred.
+ b) NITROPRUSSIDE
-- 1) NITROPRUSSIDE/INDICATIONS
* a) Nitroprusside is preferred for hypertensive emergencies (emergent need to lower mean BP 30 percent within 30 minutes and achieve a diastolic BP of 100 mmHg or less within one hour).
-- 2) NITROPRUSSIDE/DOSE
* a) 0.1 to 5 microgram/kilogram/minute intravenous infusion; up to 10 micrograms/kilogram/minute may be required (AHA, 2002).
-- 3) NITROPRUSSIDE/SOLUTION PREPARATION
* a) Dilute a 50-milligram vial in 500 milliliters of dextrose 5 percent in water (100 micrograms/milliliter). Prepare fresh every 24 hours; wrap in aluminum foil. Discard discolored solution.
-- 4) NITROPRUSSIDE/MAJOR ADVERSE REACTIONS
* a) Severe hypotension; cyanide toxicity; methemoglobinemia; lactic acidosis; chest pain or dysrhythmias (high doses).
-- 5) NITROPRUSSIDE/MONITORING PARAMETERS
* a) Monitor blood pressure every 30 to 60 seconds at onset of drip; once stabilized, monitor every 30 minutes.
+ c) NITROGLYCERIN
-- 1) In theory, nitroglycerin may help alleviate the serotonin syndrome through nitric oxide mediated downregulation of serotonin.
-- 2) ADULT - Begin continuous infusion at 5 micrograms/minute and titrate to desired effect.
-- 3) CHILD - Begin infusion at 0.25 to 0.5 micrograms/kilogram/minute and titrate to desired effect.
o 3) HYPOTENSION
+ a) Administer 10 to 20 milliliters/kilogram 0.9% saline bolus and place patient in Trendelenburg position. Further fluid therapy should be guided by central venous pressure or right heart catheterization to avoid volume overload.
+ b) Pressor agents with dopaminergic effects may theoretically worsen serotonin syndrome and should be used with caution.
+ c) DOPAMINE
-- 1) PREPARATION: Add 200 or 400 milligrams to 250 milliliters of normal saline or dextrose 5% in water to produce 800 or 1600 micrograms per milliliter or add 400 milligrams to 500 milliliters of normal saline or dextrose 5% in water to produce 800 micrograms per milliliter.
-- 2) DOSE: Begin at 2 to 5 micrograms per kilogram per minute progressing in 5 to 10 micrograms per kilogram per minute increments as needed.
-- 3) CAUTION: If VENTRICULAR ARRHYTHMIAS occur, decrease rate of administration.
+ d) NOREPINEPHRINE
-- 1) PREPARATION: Add 4 milliliters of 0.1 percent solution to 1000 milliliters of dextrose 5% in water to produce 4 micrograms/milliliter.
-- 2) INITIAL DOSE
* a) ADULTS: 2 to 3 milliliters (8 to 12 micrograms)/minute
* b) ADULT AND CHILD: 0.1 to 0.2 microgram/kilogram/minute. Titrate to maintain adequate blood pressure.
-- 3) MAINTENANCE DOSE
* a) 0.5 to 1 milliliter (2 to 4 micrograms)/minute
o 4) SEIZURES
+ a) DIAZEPAM
-- 1) MAXIMUM RATE: Administer diazepam intravenously over 2 to 3 minutes (maximum rate = 5 milligrams/minute).
-- 2) ADULT DIAZEPAM DOSE: 5 to 10 milligrams initially, repeat every 5 to 10 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 30 milligrams.
-- 3) PEDIATRIC DIAZEPAM DOSE: 0.2 to 0.5 milligram per kilogram, repeat every 5 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 10 milligrams in children over 5 years or 5 milligrams in children under 5 years of age.
-- 4) RECTAL USE: If an intravenous line cannot be established, diazepam may be given per rectum (not FDA approved), or lorazepam may be given intramuscularly.
+ b) LORAZEPAM
-- 1) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 milligrams/minute (Prod Info Ativan(R), 1991).
-- 2) ADULT LORAZEPAM DOSE: 2 to 4 milligrams intravenously. Initial doses may be repeated in 10 to 15 minutes if seizures persist (Prod Info Ativan(R), 1999).
-- 3) PEDIATRIC LORAZEPAM DOSE: 0.05 to 0.1 milligram/kilogram intravenously, repeated twice at intervals of 15 to 20 minutes (Benitz & Tatro, 1988)(Giang & McBride, 1988).
+ c) RECURRING SEIZURES: If seizures cannot be controlled with diazepam or recur, give phenobarbital.
+ d) PHENOBARBITAL
-- 1) SERUM LEVEL MONITORING: Monitor serum levels over next 12 to 24 hours for maintenance of therapeutic levels (15 to 25 micrograms per milliliter).
-- 2) ADULT PHENOBARBITAL LOADING DOSE: 600 to 1200 milligrams of phenobarbital intravenously initially (10 to 20 milligrams per kilogram) diluted in 60 milliliters of 0.9 percent saline given at 25 to 50 milligrams per minute.
-- 3) ADULT PHENOBARBITAL MAINTENANCE DOSE: Additional doses of 120 to 240 milligrams may be given every 20 minutes.
-- 4) MAXIMUM SAFE ADULT PHENOBARBITAL DOSE: No maximum safe dose has been established. Patients in status epilepticus have received as much as 100 milligrams/minute until seizure control was achieved or a total dose of 10 milligrams/kilogram.
-- 5) PEDIATRIC PHENOBARBITAL LOADING DOSE: 15 to 20 milligrams per kilogram of phenobarbital intravenously at a rate of 25 to 50 milligrams per minute.
-- 6) PEDIATRIC PHENOBARBITAL MAINTENANCE DOSE: Repeat doses of 5 to 10 milligrams per kilogram may be given every 20 minutes.
-- 7) MAXIMUM SAFE PEDIATRIC PHENOBARBITAL DOSE: No maximum safe dose has been established. Children in status epilepticus have received doses of 30 to 120 milligrams/kilogram within 24 hours. Vasopressors and mechanical ventilation were needed in some patients receiving these doses.
-- Cool

NEONATAL PHENOBARBITAL LOADING DOSE: 20 to 30 milligrams/kilogram intravenously at a rate of no more than 1 milligram/kilogram per minute in patients with no preexisting phenobarbital serum levels.
-- 9) NEONATAL PHENOBARBITAL MAINTENANCE DOSE: Repeat doses of 2.5 milligrams/kilogram every 12 hours may be given; adjust dosage to maintain serum levels of 20 to 40 micrograms/milliliter.
-- 10) MAXIMUM SAFE NEONATAL PHENOBARBITAL DOSE: Doses of up to 20 milligrams/kilogram/minute up to a total of 30 milligrams/kilogram have been tolerated in neonates.
-- 11) CAUTIONS: Adequacy of ventilation must be continuously monitored in children and adults. Intubation may be necessary with increased doses.
o 5) CYPROHEPTADINE
+ a) Cyproheptadine is a non-specific 5-HT antagonist that has been shown to block development of serotonin syndrome in animals (Sternbach, 1991). Cyproheptadine has been used in the treatment of serotonin syndrome (Mills, 1997)(Goldberg & Huk, 1992). There are no controlled human trials substantiating its efficacy.
+ b) ADULT - 4 to 8 milligrams orally repeated every 1 to 4 hours until therapeutic response is observed or maximum of 32 milligrams administered (Mills, 1997).
+ c) CHILD - 0.25 milligram/kilogram/day divided every 6 hours, maximum dose 12 milligrams/day (Mills, 1997).
o 6) PROPRANOLOL
+ a) Propranolol is a 5-HT1A receptor antagonist (Sternbach, 1991). Propranolol has been used in human cases of serotonin syndrome with apparent benefit (Guze & Baxter, 1986)(Dursun et al, 1997). There are no controlled human trials substantiating its efficacy.
+ b) PROPRANOLOL/ADULT DOSE
-- 1) 1 milligram/dose intravenously, administered no faster than 1 milligram/minute repeated every 2 to 5 minutes until desired response is seen or a maximum of 5 milligrams has been given.
+ c) PROPRANOLOL/PEDIATRIC DOSE
-- 1) 0.01 to 0.1 milligram/kilogram/dose over 10 minutes. Maximum 1 milligram/dose (Benitz & Tatro, 1988).
o 7) CHLORPROMAZINE -
+ a) Chlorpromazine is a 5-HT2 receptor antagonist that has been used to treat cases of serotonin syndrome (Graham, 1997) Gillman, 1996). Controlled human trial documenting its efficacy are lacking.
+ b) ADULT - 25 to 100 milligrams intramuscularly repeated in one hour if necessary.
+ c) CHILD - 0.5 to 1 milligram/kilogram repeated as needed every 6 to 12 hours not to exceed 2 milligrams/kilogram/day.
o Cool

OTHER
+ a) Other agents which have been used to treat serotonin syndrome include methysergide and mirtazapine (Mills, 1997) Hoes, 1996).
o 9) NOT RECOMMENDED
+ a) BROMOCRIPTINE - Is used in the treatment of neuroleptic malignant syndrome but is NOT RECOMMENDED in the treatment of serotonin syndrome as it has serotonergic effects (Gillman, 1997). In one case the use of bromocriptine was associated with a fatal outcome (Kline et al, 1989).
* O) FLUMAZENIL
o 1) Flumazenil is NOT recommended because of the risk of seizures.
o 2) An experimental animal model found an increased risk of death from unmasked seizures when rats received flumazenil following intoxication with cocaine and diazepam (Derlet & Albertson, 1994).
o 6.6 PARENTERAL EXPOSURE
+ 6.6.2 TREATMENT
-- A) INTRA-ARTERIAL INFUSION
* 1) Continuous axillary brachial plexus block with 0.5 percent bupivacaine was effective in relieving ischemia after inadvertent humeral intraarterial injection of cocaine one hour earlier (Berger et al, 1988).
* 2) Heparin and intravenous or intraarterial nitroprusside have been effective in the treatment of vasospasm due to intraarterial injection of amphetamines.
* 3) Some authors suggest that phentolamine may be the agent of choice in the reversal of vasoconstriction induced by injection of a sympathomimetic agent (Shukla, 1993).
-- B) GENERAL TREATMENT
* 1) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.
-- C) Treatment should include recommendations li