среда, 20 декабря 2017 г.

cocktail_dose

Myer's (Intravenous) Cocktail

Reproduced by permission of Dr. Jonathan Wright

  • Magnesium chloride hexahydrate 20% 2-5 cc
  • Calcium gluconate 10% 1-4 cc
  • Hydroxy-cobalamine 1000 mcg./cc 1 cc
  • Pyridoxine hydrochloride 100 mg./cc 1 cc
  • Dexpanthenol 250 mg./cc 1 cc
  • B-complex 100 1 cc
  • Vitamin C 222 mg./cc 1-30 cc
  • Sterile water to isotonicity: 280-320 mOsm/ml.
  • 1 cc sterile water /cc of calcium gluconate
  • 1 cc calcium gluconate/2 cc magnesium chloride unless anxiety or migraines, then go to 1:1.

  • All nutrients in one syringe and push in over 5-15 minutes through a 25G butterfly.
  • If pain on injection cut with sterile water to 50%
  • Too rapid magnesium can cause severe hypotension.
  • Watch for and correct hypokalemia before administering Myer's cocktail. Suspect hypokalemia in people on diuretics, beta-agonists, corticosteroids, or diarrhea.
  • Measure serum potassium. When in doubt give 25 mEq. of potassium orally at the time of the injection and repeat 4-6 hours later.

These nutritional protocols are for doctors practicing nutritional medicine. They are based on clinical experience and a review of the nutritional literature. They should be correlated with your knowledge and clinical experience and used at your own responsibility.

Offsite Research Articles:

Alternative Medicine Review 2002 Oct;7(5):389-403

This paper presents a rationale for the therapeutic use of intravenous nutrients, reviews the relevant published clinical research, describes the author's clinical experiences, and discusses potential side effects and precautions.

Updated on: Apr. 18, 2013

The Chronicles of Nausea

by Ashli McCall

Beyond Morning Sickness

Management of the Acute Migraine Headache

GLEN AUKERMAN, M.D., DOUG KNUTSON, M.D., and WILLIAM F. MISER, M.D., M.A.

Ohio State University College of Medicine and Public Health, Columbus, Ohio

Am Fam Physician. 2002 Dec 1;66(11):2123-2131.

Patient Information Handout

Related Editorial

Article Sections

As many as 30 million Americans have migraine headaches. The impact on patients and their families can be tremendous, and treatment of migraines can present diagnostic and therapeutic challenges for family physicians. Abortive treatment options include nonspecific and migraine-specific therapy. Nonspecific therapies include analgesics (aspirin, nonsteroidal anti-inflammatory drugs, and opiates), adjunctive therapies (antiemetics and sedatives), and other nonspecific medications (intranasal lidocaine or steroids). Migraine-specific abortive therapies include ergotamine and its derivatives, and triptans. Complementary and alternative therapies can also be used to abort the headache or enhance the efficacy of another therapeutic modality. Treatment choices for acute migraine should be based on headache severity, migraine frequency, associated symptoms, and comorbidities.

Migraine headaches are a major public health problem affecting more than 28 million persons in this country.1 Nearly 25 percent of women and 9 percent of men experience disabling migraines.2 , 3 The impact of these headaches on patients and their families is tremendous, with many patients reporting frequent and significant disability.4 The economic burden of migraine headaches in the United States is also tremendous. Persons with migraines lose an average of four to six work days each year, with an annual total loss nationwide of 64 to 150 million work days. The estimated direct and indirect costs of migraine approach $17 billion.5 , 6 Despite the prevalence of migraines and the availability of multiple treatment options, this condition is often undiagnosed and untreated.7 About one half of patients stop seeking medical care for their migraines, in part because of dissatisfaction with the therapy they have received.4

Patients with migraine headaches often present family physicians with diagnostic and therapeutic challenges. The aspects of migraine management that deserve careful consideration include the treatment of acute pain, the role of neuroimaging, and the management of patients who fail to respond to initial treatment. This article addresses these issues, presenting the evidence-based migraine headache treatment guidelines recently established by the U.S. Headache Consortium, a multidisciplinary team consisting of members from seven organizations, including the American Academy of Family Physicians (AAFP). The guidelines are available on the AAFP Web site.8

Clinical Presentation

The classification of migraines is based on the clinical features of the headache, most notably the presence or absence of a characteristic aura before the onset of pain. The aura may take many forms but usually involves visual distortions, including scotomas. Other prodromal symptoms described by many patients with migraines include nausea, food cravings, heightened sensory perceptions, and alterations in mood or behavior.

The International Headache Society's categorization of headaches is listed in Table 1 .9 Migraines can be triggered by hormonal changes, certain foods, sensory stimuli (i.e., light, smells), missed meals, or the relief of tension after stressful events.

International Headache Society Classification of Headaches

Migraine headache—diagnostic requirements

At least two of the following features:

Worsening pain with routine activity

Moderate to severe intensity

At least one of the following features:

Nausea and/or vomiting

Photophobia and phonophobia

Tension headache—diagnostic requirements

At least two of the following features:

Pressing, tightening, or nonpulsatile character

Mild to moderate intensity

No aggravation with routine activity

Both of the following features:

No nausea or vomiting (may have anorexia)

No photophobia and phonophobia (but may have one or the other)

Cluster headache—diagnostic requirements

Five attacks, with a frequency of one to eight attacks on any given day

Severe unilateral, bilateral, supraorbital, or temporal pain lasting 15 to 180 minutes (untreated), with at least one of the following features on the same side as the pain:

Forehead and/or facial sweating

Adapted with permission from Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Headache Classification Committee of the International Headache Society. Cephalalgia 1988;8 Suppl 7:1–96 .

International Headache Society Classification of Headaches

Migraine headache—diagnostic requirements

At least two of the following features:

Worsening pain with routine activity

Moderate to severe intensity

At least one of the following features:

Nausea and/or vomiting

Photophobia and phonophobia

Tension headache—diagnostic requirements

At least two of the following features:

Pressing, tightening, or nonpulsatile character

Mild to moderate intensity

No aggravation with routine activity

Both of the following features:

No nausea or vomiting (may have anorexia)

No photophobia and phonophobia (but may have one or the other)

Cluster headache—diagnostic requirements

Five attacks, with a frequency of one to eight attacks on any given day

Severe unilateral, bilateral, supraorbital, or temporal pain lasting 15 to 180 minutes (untreated), with at least one of the following features on the same side as the pain:

Forehead and/or facial sweating

Adapted with permission from Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Headache Classification Committee of the International Headache Society. Cephalalgia 1988;8 Suppl 7:1–96 .

Evaluation

The initial task in managing a patient who presents with migraine headache is to take a detailed history and perform a thorough physical and neurologic examination. Patients may present with significant expectations derived from the numerous sources of information available, especially those on the Internet. One of the most popular and authoritative Web sites is that of the National Headache Foundation (NHF) (http://www.headaches.org/). The NHF site provides patients with a “checklist” of questions that primary care physicians should ask when taking an appropriate history (Table 2) .10

Questions to Ask Patients About Their Headaches

How frequent are the headaches?

What time of day do the headaches occur?

In women, do the headaches occur during the menstrual cycle?

What is the character of the pain: dull, aching, throbbing, piercing, squeezing, excruciating?

What other symptoms accompany the headache? Nausea or vomiting? Dizziness? Head/neck muscles contracting? Are the senses (eyesight, hearing, touch) affected?

Where is the pain located? One or both sides of the head? Front or back of the head? Over or behind one eye?

How long do the headaches last? Hours, days?

Do you take over-the-counter medications for your headaches? Did another doctor prescribe a medication? Does it work and for how long? Do you take any natural remedies or herbs?

Where are you when the headaches occur? Home, office, shopping, etc.?

Do the headaches ever occur during sexual activity?

When you have these headaches, are you under any stress?

What is the weather like when the headaches occur? Are you exposed to any odors such as perfume, chemicals, or smoke when the headaches occur?

When the headaches occur, have you eaten a meal or snack recently, or have you missed a meal? If you have eaten, what foods did you eat and what beverages did you drink within the past 24 hours?

What are your sleeping patterns? Do these headaches ever awaken you from sleep?

Is there a history of headaches in your family?

Have you ever been evaluated for these headaches? If so, what was the result?

Information from Moore KL, Noble SL. Drug treatment of migraine: part I. Acute therapy and drug-rebound headache. Am Fam Physician 1997;56:2039–48 .

Questions to Ask Patients About Their Headaches

How frequent are the headaches?

What time of day do the headaches occur?

In women, do the headaches occur during the menstrual cycle?

What is the character of the pain: dull, aching, throbbing, piercing, squeezing, excruciating?

What other symptoms accompany the headache? Nausea or vomiting? Dizziness? Head/neck muscles contracting? Are the senses (eyesight, hearing, touch) affected?

Where is the pain located? One or both sides of the head? Front or back of the head? Over or behind one eye?

How long do the headaches last? Hours, days?

Do you take over-the-counter medications for your headaches? Did another doctor prescribe a medication? Does it work and for how long? Do you take any natural remedies or herbs?

Where are you when the headaches occur? Home, office, shopping, etc.?

Do the headaches ever occur during sexual activity?

When you have these headaches, are you under any stress?

What is the weather like when the headaches occur? Are you exposed to any odors such as perfume, chemicals, or smoke when the headaches occur?

When the headaches occur, have you eaten a meal or snack recently, or have you missed a meal? If you have eaten, what foods did you eat and what beverages did you drink within the past 24 hours?

What are your sleeping patterns? Do these headaches ever awaken you from sleep?

Is there a history of headaches in your family?

Have you ever been evaluated for these headaches? If so, what was the result?

Information from Moore KL, Noble SL. Drug treatment of migraine: part I. Acute therapy and drug-rebound headache. Am Fam Physician 1997;56:2039–48 .

This site can be a highly useful part of patient education, but family physicians should be aware that it advises patients to seek referral to a subspecialist or headache clinic if the primary care physician does not appear to appropriately appreciate, diagnose, or treat the headache. This suggestion may raise concern in some patients about the ability of primary care physicians to appropriately manage headaches. Family physicians might ask patients about their sources of medical information.

Physicians may struggle to determine the appropriate use of neuroimaging in the patient with migraine. The American Academy of Neurology suggests that neuroimaging should be considered only in patients with migraine who have atypical headache patterns or neurologic signs11; the U.S. Headache Consortium has developed evidence-based guidelines on the use of neuroimaging for patients with migraines.

In general, the U.S. Headache Consortium guidelines do not recommend neuroimaging if the patient is not at higher risk of a significant abnormality than the general population or if the results of the study would not change the management of the headache. Symptoms that increase the odds of positive neuroimaging results include rapidly increasing frequency of headache, a history of uncoordination, focal neurologic signs or symptoms, and a headache that awakens the patient from sleep. Other “red flags” include abrupt onset of severe headache, marked change in headache pattern, or persistent headache following head trauma. The specific U.S. Headache Consortium guidelines for neuroimaging are outlined in Table 3 .12

Guidelines for Neuroimaging in Patients Presenting With Migraine Headaches

In patients with nonacute headache and unexplained findings on neurologic examination, neuroimaging should be considered.

In patients with neurologic symptoms (headache that is worsened with use of Valsalva's maneuver, awakens the patient from sleep, is newly onset in an older person, or is progressively worsening), the evidence is insufficient to make specific recommendations. The conservative approach would be to consider neuroimaging in these patients.

In patients with a normal neurologic examination, neuroimaging is usually not warranted. However, if the headache has atypical features or does not meet the strict definition of migraine, a lower threshold may apply.

Information from reference 12 .

Guidelines for Neuroimaging in Patients Presenting With Migraine Headaches

In patients with nonacute headache and unexplained findings on neurologic examination, neuroimaging should be considered.

In patients with neurologic symptoms (headache that is worsened with use of Valsalva's maneuver, awakens the patient from sleep, is newly onset in an older person, or is progressively worsening), the evidence is insufficient to make specific recommendations. The conservative approach would be to consider neuroimaging in these patients.

In patients with a normal neurologic examination, neuroimaging is usually not warranted. However, if the headache has atypical features or does not meet the strict definition of migraine, a lower threshold may apply.

Information from reference 12 .

Electroencephalography is not useful in the routine evaluation of patients with headache but may be appropriate in those who have associated symptoms suggestive of a seizure disorder, atypical migrainous aura, or episodic loss of consciousness.13

Goals of Migraine Treatment

Migraine treatment depends on the duration and severity of pain, associated symptoms, degree of disability, and initial response to therapy. Management of migraines can be difficult because of the complexity of migraines and the variation of symptoms among and within patients. Some medical conditions (stroke, myocardial infarction, epilepsy, affective and anxiety disorders, and some connective tissue disorders) are more common in people with migraine. These conditions provide opportunities to treat both conditions with one medication but are also limiting because of drug interactions or contraindications. Appropriate migraine therapy should allow for consideration of the above factors.14

The U.S. Headache Consortium identified the goals of long-term migraine treatment and successful management of acute migraine (Tables 4 and 5) .14 These goals emphasize the importance of patient education and self-participation in the management of migraines, and of establishing reasonable patient expectations and effective communication. Of note, these treatment goals are also designed to avoid “rebound” or medication-overuse headaches. Frequent use of some migraine medications (e.g., ergotamine [Ergostat], opiates, analgesics, and triptans) may cause medication-overuse headaches. Preventive therapy should be considered if the patient has more than two headaches per week.15

U.S. Headache Consortium Guidelines for Migraine Treatment

Goals of long-term migraine treatment

Goals for successful treatment of acute migraine attacks

Reduce migraine frequency and severity

Treat migraine attacks rapidly and consistently without recurrence

Restore the patient's ability to function

Improve quality of life

Minimize the use of back-up and rescue medications*

Optimize self-care for overall management

Avoid escalation of headache medication use

Be cost-effective in overall management

Educate and enable patients to manage their disease

Cause minimal or no adverse effects

*— Rescue medications are defined as medications used at home when other treatments fail that permit the patient to get relief without a visit to the physician's office or emergency department . 11

Information from reference 14 .

U.S. Headache Consortium Guidelines for Migraine Treatment

Goals of long-term migraine treatment

Goals for successful treatment of acute migraine attacks

Reduce migraine frequency and severity

Treat migraine attacks rapidly and consistently without recurrence

Restore the patient's ability to function

Improve quality of life

Minimize the use of back-up and rescue medications*

Optimize self-care for overall management

Avoid escalation of headache medication use

Be cost-effective in overall management

Educate and enable patients to manage their disease

Cause minimal or no adverse effects

*— Rescue medications are defined as medications used at home when other treatments fail that permit the patient to get relief without a visit to the physician's office or emergency department . 11

Information from reference 14 .

Overview of Acute Pain Management in Patients With Migraine Headaches

For mild to moderate migraine attacks or severe attacks that have been responsive in the past to similar agents, use the following options:

Combination analgesics containing caffeine

For moderate to severe migraine or mild to moderate migraines that respond poorly to NSAIDs, use:

Migraine-specific drugs (i.e., triptans [naratriptan, rizatriptan, sumatriptan, zolmitriptan], DHE)

Combination drug therapy (e.g., aspirin plus acetaminophen* plus caffeine)

Other drugs such as ergotamine

For migraine accompanied by nausea or vomiting, use a non-oral route of administration.

For severe migraine that does not respond to other treatments, use a self-administered rescue medication.

Limit and carefully monitor the use of opiates and butalbital-containing analgesics.

NSAIDs = nonsteroidal anti-inflammatory drugs; DHE = dihydroergotamine .

*— Acetaminophen alone is not recommended for migraine .

Information from reference 14 .

Overview of Acute Pain Management in Patients With Migraine Headaches

For mild to moderate migraine attacks or severe attacks that have been responsive in the past to similar agents, use the following options:

Combination analgesics containing caffeine

For moderate to severe migraine or mild to moderate migraines that respond poorly to NSAIDs, use:

Migraine-specific drugs (i.e., triptans [naratriptan, rizatriptan, sumatriptan, zolmitriptan], DHE)

Combination drug therapy (e.g., aspirin plus acetaminophen* plus caffeine)

Other drugs such as ergotamine

For migraine accompanied by nausea or vomiting, use a non-oral route of administration.

For severe migraine that does not respond to other treatments, use a self-administered rescue medication.

Limit and carefully monitor the use of opiates and butalbital-containing analgesics.

NSAIDs = nonsteroidal anti-inflammatory drugs; DHE = dihydroergotamine .

*— Acetaminophen alone is not recommended for migraine .

Information from reference 14 .

If identified early, a migraine may be aborted with pharmacologic treatment using either nonspecific or migraine-specific medications. Gastrointestinal motility is reduced during acute migraine, causing impaired drug absorption. If administration of oral medication is not possible because of nausea or if the oral agents fail, alternative methods of administration (rectal, nasal, subcutaneous or intravenous) may be used for many medications.

Nonspecific Abortive Migraine Therapy

Table 6 4 , 16-18 , 22 lists the nonspecific treatments that may be effective for mild to moderate migraines. Non-narcotic analgesics can be used for mild to moderate migraines that are not associated with nausea and vomiting. Administration as early as possible during an attack improves efficacy. The use of these analgesics should be closely monitored because overuse may lead to rebound headaches.

Nonspecific Medications Used to Treat Migraine Headaches

650 to 1,000 mg every four to six hours

G6PD-deficiency, bleeding disorder

GI upset; suppositories may cause rectal irritation

Maximal initial dose: 1 g

Maximal daily dosage: 4 g

400 to 800 mg every six hours

Dizziness, rash, GI upset

Maximal initial dose: 800 mg

Avoid taking more than 2.4 g per day

Naproxen sodium (Anaprox)

275 to 550 mg every two to six hours

Dizziness, rash, pruritus, GI upset, constipation

Maximal initial dose: 825 mg

Avoid taking more than 1.5 g per day

60 mg IM every 15 to 30 minutes

Aspirin/NSAID-induced asthma, pregnancy, cerebrovascular hemorrhage

Edema, drowsiness, dizziness, GI upset, increased diaphoresis

Maximal dosage: 120 mg per day

Treatment not to exceed five days

50 to 150 mg IM or IV

MAOI use within 15 days, pregnancy, lactation

Hypotension, fatigue, drowsiness, dizziness, nausea, vomiting, constipation, muscle weakness, histamine release, respiratory depression

Repeat 50 to 150 mg every three to four hours

One spray (1 mg) in one nostril

Use with caution in patients with impaired renal, hepatic, or pulmonary function, elderly patients, those with CNS depression

Repeat in one hour if needed

Maximal daily doses: four

Limit use to two days per week

10 mg IV or orally 20 to 30 minutes before or with a simple analgesic, NSAID, or ergotamine derivative

Pheochromocytoma, seizure disorder, GI bleeding, GI obstruction

Restlessness, drowsiness, diarrhea, muscle weakness, dystonic reaction

25 mg orally or suppository

CNS depression, use of adrenergic blocker

Hypotension, tachycardia, arrhythmias, akathisia, pseudo-parkinsonism, tardive dyskinesia, dystonia, dizziness, xerostomia, constipation, urinary retention, blurred vision, pigmentary retinopathy, nasal congestion, decreased diaphoresis

Maximum of three doses per 24 hours

Isometheptene, acetaminophen, dichloralphenazone (Midrin)

Maximal initial dose: two capsules

Hepatic or renal impairment, diabetes, hypertension, glaucoma, alcoholism, cardiac disease, MAOI use within 14 days

Hypertension, dizziness, rash

Repeat one capsule per hour to maximal dosage of five capsules per 12 hours and 20 per month; limit use to two days or fewer per week

NSAIDs = nonsteroidal anti-inflammatory drugs; G6PD = glucose-6-phosphate dehydrogenase; GI = gastrointestinal; IM = intramuscularly; IV = intravenously; MAOI = monoamine oxidase inhibitor; CNS = central nervous system .

*— Efficacy = clinical impression of effectiveness on a scale of 1 to 4, with 4 being most effective .

Information from references 4 , 16 through 18, and 22 .

Nonspecific Medications Used to Treat Migraine Headaches

650 to 1,000 mg every four to six hours

G6PD-deficiency, bleeding disorder

GI upset; suppositories may cause rectal irritation

Maximal initial dose: 1 g

Maximal daily dosage: 4 g

400 to 800 mg every six hours

Dizziness, rash, GI upset

Maximal initial dose: 800 mg

Avoid taking more than 2.4 g per day

Naproxen sodium (Anaprox)

275 to 550 mg every two to six hours

Dizziness, rash, pruritus, GI upset, constipation

Maximal initial dose: 825 mg

Avoid taking more than 1.5 g per day

60 mg IM every 15 to 30 minutes

Aspirin/NSAID-induced asthma, pregnancy, cerebrovascular hemorrhage

Edema, drowsiness, dizziness, GI upset, increased diaphoresis

Maximal dosage: 120 mg per day

Treatment not to exceed five days

50 to 150 mg IM or IV

MAOI use within 15 days, pregnancy, lactation

Hypotension, fatigue, drowsiness, dizziness, nausea, vomiting, constipation, muscle weakness, histamine release, respiratory depression

Repeat 50 to 150 mg every three to four hours

One spray (1 mg) in one nostril

Use with caution in patients with impaired renal, hepatic, or pulmonary function, elderly patients, those with CNS depression

Repeat in one hour if needed

Maximal daily doses: four

Limit use to two days per week

10 mg IV or orally 20 to 30 minutes before or with a simple analgesic, NSAID, or ergotamine derivative

Pheochromocytoma, seizure disorder, GI bleeding, GI obstruction

Restlessness, drowsiness, diarrhea, muscle weakness, dystonic reaction

25 mg orally or suppository

CNS depression, use of adrenergic blocker

Hypotension, tachycardia, arrhythmias, akathisia, pseudo-parkinsonism, tardive dyskinesia, dystonia, dizziness, xerostomia, constipation, urinary retention, blurred vision, pigmentary retinopathy, nasal congestion, decreased diaphoresis

Maximum of three doses per 24 hours

Isometheptene, acetaminophen, dichloralphenazone (Midrin)

Maximal initial dose: two capsules

Hepatic or renal impairment, diabetes, hypertension, glaucoma, alcoholism, cardiac disease, MAOI use within 14 days

Hypertension, dizziness, rash

Repeat one capsule per hour to maximal dosage of five capsules per 12 hours and 20 per month; limit use to two days or fewer per week

NSAIDs = nonsteroidal anti-inflammatory drugs; G6PD = glucose-6-phosphate dehydrogenase; GI = gastrointestinal; IM = intramuscularly; IV = intravenously; MAOI = monoamine oxidase inhibitor; CNS = central nervous system .

*— Efficacy = clinical impression of effectiveness on a scale of 1 to 4, with 4 being most effective .

Information from references 4 , 16 through 18, and 22 .

Acetaminophen alone has not been shown to be beneficial in migraine treatment, but it is effective in combination with aspirin and caffeine. Ketorolac (Toradol), a parenteral nonsteroidal anti-inflammatory drug (NSAID), has a relatively rapid onset of action and a duration of approximately six hours. It is generally reserved for abortive therapy of severe migraines, and rebound headache is unlikely. Opioid analgesics such as meperidine (Demerol) and butorphanol (Stadol) are sometimes required to abort severe migraines. Narcotic use should be avoided for chronic daily headaches because it can lead to dependency, rebound headaches, and eventual loss of efficacy.

Adjunctive therapy is used to treat the associated symptoms of migraine and provide synergistic analgesia. While metoclopramide (Reglan) is sometimes recommended as a single agent in the treatment of migraine pain, its main use is for treating accompanying nausea and improving gastric motility, which may be impaired during migraine attacks. Prochlorperazine (Compazine) can effectively relieve headache pain.19 , 20 Other adjunctive therapies for the abortive treatment of migraines are caffeine and sleep.

The combination of isometheptene, acetaminophen, and dichloralphenazone (Midrin) has been shown to be effective in the treatment of milder migraine headaches.10 , 21 Sedatives such as the barbiturates have historically been used to induce sleep in persons with migraines. However, with the advent of effective nonsedating agents and migraine-specific therapy, sedatives are no longer widely used in migraine therapy.

Other nonspecific therapies that have been used to abort acute migraine attacks include intranasal lidocaine (Xylocaine) and systemic steroids. While limited studies report lidocaine to be superior to placebo, the reported incidence of recurrent headaches has been inconsistent. Because the evidence is insufficient, a defined role for intranasal lidocaine as abortive migraine therapy has yet to be established. Steroid therapy may be the treatment of choice for patients with status migrainosus (a severe, continuous migraine that may last up to one week), but there are no good studies documenting its efficacy in the treatment of the acute migraine attack.14

Specific Abortive Migraine Therapy

ERGOTAMINE AND ITS DERIVATIVES

Historically, ergotamine, a 5-hydroxytryptamine (5-HT1) nonselective agonist, was the standard abortive migraine therapy. It now has a more limited use because of its potential for causing medication-overuse headaches and increasing the frequency of headaches, ergot poisoning, and negative effects on migraine prophylactic medications. The effectiveness of ergotamine depends on its administration at the onset of migraine pain.22

Oral preparations combining ergotamine and caffeine (Cafergot) are available, as are rectal suppositories. Dihydroergotamine (DHE), a semisynthetic ergot alkaloid and nonselective 5-HT1 receptor agonist, is considered to be more appropriate for the treatment of severe migraines. It is available in parenteral preparations and as a nasal spray. Like ergotamine, DHE has oxytocic properties, precluding its use in pregnancy. Because of their ability to cause peripheral vasoconstriction, ergot alkaloids should not be used chronically. The ergotamine derivatives used to treat migraines are described in Table 7 .4 , 16-18 , 22

A widely prescribed and effective class of medications for migraines is the 5-HT1 receptor-specific agonists (“triptans”). The use of triptans in the treatment of migraine headaches is described in Table 7 .4 , 10 , 16-18 Triptans are usually reserved for use in patients with moderate to severe migraines or mild to moderate migraines that are unresponsive to analgesics or NSAIDs. As a class, triptans are usually well tolerated. Contraindications to their use include ischemic vascular conditions, vasospastic coronary disease, uncontrolled hypertension, or other significant cardiovascular disease. While members of the triptan family are similar in many ways, there are significant differences in time to peak blood concentration and half-life.

Migraine-Specific Medications

1 to 2 mg orally every hour, maximum of three doses in 24 hours Use lowest effective dose Suppository: 1 mg, maximal dosage, two to three per day and 12 per month

Use of triptans, pregnancy, lactation

Increased incidence of migraines, daily headaches, ergot poisoning, tachycardia, bradycardia, arterial spasm, localized edema, numbness and tingling in extremities, nausea, vomiting, diarrhea, xerostomia

Caffeine plus ergotamine (Cafergot)

Two tablets (100 mg caffeine/1 mg ergotamine) at onset, then one tablet every 30 minutes, up to six tablets per attack, 10 per week Suppository (2 mg ergotamine/100 mg caffeine), one at onset, one in one hour as needed; maximal dosage, two per attack

Use of triptans

Severe reactions: myocardial infarction, myocardial or pleuropulmonary fibrosis, vasospastic ischemia Common reactions: dizziness, rash

1 mg IM, SC Maximal initial dose: 0.5 to 1.0 mg; can be repeated every hour to maximal dosage of 3 mg IM or 2 mg IV per day, and 6 mg per week Intranasal: one 0.5-mg spray in each nostril, followed by one spray in each nostril 15 minutes later; maximal dosage: four sprays (2 mg) per day

Triptans, beta blockers, antihypertensives, methysergide (Sansert), SSRIs, dopamine (Intropin), macrolides, nitrates, angina, CAD, clarithromycin (Biaxin), hypertension, myocardial infarction, peripheral vascular disease, pregnancy, renal impairment, sepsis, breastfeeding, ergot alkaloid sensitivity

Ergot toxicity, coronary vasospasm, cardiac events including angina, myocardial infarction, ventricular tachycardia or fibrillation, hypertension, adverse cerebrovascular events, localized edema, pruritus, sinus tachycardia or bradycardia, weakness in legs, nausea, vomiting, diarrhea, drowsiness, xerostomia, local injection reaction, numbness

6 mg SC, repeated in one hour; maximal dosage, 12 mg per 24 hours 25 to 100 mg orally every two hours, maximal dosage: 200 mg per day Maximal initial dose: 100 mg Intranasal: 5 to 10 mg (one to two sprays) in one nostril; dose may be repeated after 2 hours to maximal dosage of 40 mg per day

Ergotamine, MAOIs, use within 24 hours of another triptan, hemiplegic or basilar migraine, pregnancy, impaired hepatic function, as prophylactic therapy, CAD

Nausea, warmth, vomiting, vertigo, malaise, headache, injection site reactions, chest pressure and heaviness

1.0 to 2.5 mg orally every four hours to maximal dosage of 5 mg per day

Ergot-type medications, SSRIs, oral contraceptives, smoking, CAD

Dizziness, drowsiness, nausea, vomiting, fatigue, paresthesias

Rizatriptan (Maxalt, Maxalt MLT)

5 to 20 mg orally every two hours to maximal dosage of 30 mg per day

Ergot-type medications, SSRIs, other triptans, MAOIs, propranolol (Inderal), cimetidine (Tagamet), CAD

Tachycardia, bradycardia, throat tightness, closure

2.5 to 5.0 mg orally every two hours to maximal dosage of 10 mg per 24 hours

Ergot-type medications, SSRIs, other triptans, MAOIs, CAD

IM = intramuscularly; SC = subcutaneously; IV = intravenously; SSRIs = selective serotonin reuptake inhibitors; CAD = coronary artery disease; MAOIs = monoamine oxidase inhibitors .

*— Efficacy = clinical impression of effectiveness on a scale of 1t o 4, with 4 being the most effective .

†— Avoid chronic use because of potential for peripheral vasoconstriction .

‡— Frovatriptan (Frova) and almotriptan (Axert) have been released since the article was researched, but generally offer no significant advantages or disadvantages to the trip-tans listed above. Eletriptan is in development .

note : This table is not all-inclusive in treatment protocols, contraindications or adverse reactions. Physicians should consult current Physician's Desk Reference and other pharmacologic resources before prescribing . 16-18 , 22

Information from references 4 , 16 through 18, and 22 .

Migraine-Specific Medications

1 to 2 mg orally every hour, maximum of three doses in 24 hours Use lowest effective dose Suppository: 1 mg, maximal dosage, two to three per day and 12 per month

Use of triptans, pregnancy, lactation

Increased incidence of migraines, daily headaches, ergot poisoning, tachycardia, bradycardia, arterial spasm, localized edema, numbness and tingling in extremities, nausea, vomiting, diarrhea, xerostomia

Caffeine plus ergotamine (Cafergot)

Two tablets (100 mg caffeine/1 mg ergotamine) at onset, then one tablet every 30 minutes, up to six tablets per attack, 10 per week Suppository (2 mg ergotamine/100 mg caffeine), one at onset, one in one hour as needed; maximal dosage, two per attack

Use of triptans

Severe reactions: myocardial infarction, myocardial or pleuropulmonary fibrosis, vasospastic ischemia Common reactions: dizziness, rash

1 mg IM, SC Maximal initial dose: 0.5 to 1.0 mg; can be repeated every hour to maximal dosage of 3 mg IM or 2 mg IV per day, and 6 mg per week Intranasal: one 0.5-mg spray in each nostril, followed by one spray in each nostril 15 minutes later; maximal dosage: four sprays (2 mg) per day

Triptans, beta blockers, antihypertensives, methysergide (Sansert), SSRIs, dopamine (Intropin), macrolides, nitrates, angina, CAD, clarithromycin (Biaxin), hypertension, myocardial infarction, peripheral vascular disease, pregnancy, renal impairment, sepsis, breastfeeding, ergot alkaloid sensitivity

Ergot toxicity, coronary vasospasm, cardiac events including angina, myocardial infarction, ventricular tachycardia or fibrillation, hypertension, adverse cerebrovascular events, localized edema, pruritus, sinus tachycardia or bradycardia, weakness in legs, nausea, vomiting, diarrhea, drowsiness, xerostomia, local injection reaction, numbness

6 mg SC, repeated in one hour; maximal dosage, 12 mg per 24 hours 25 to 100 mg orally every two hours, maximal dosage: 200 mg per day Maximal initial dose: 100 mg Intranasal: 5 to 10 mg (one to two sprays) in one nostril; dose may be repeated after 2 hours to maximal dosage of 40 mg per day

Ergotamine, MAOIs, use within 24 hours of another triptan, hemiplegic or basilar migraine, pregnancy, impaired hepatic function, as prophylactic therapy, CAD

Nausea, warmth, vomiting, vertigo, malaise, headache, injection site reactions, chest pressure and heaviness

1.0 to 2.5 mg orally every four hours to maximal dosage of 5 mg per day

Ergot-type medications, SSRIs, oral contraceptives, smoking, CAD

Dizziness, drowsiness, nausea, vomiting, fatigue, paresthesias

Rizatriptan (Maxalt, Maxalt MLT)

5 to 20 mg orally every two hours to maximal dosage of 30 mg per day

Ergot-type medications, SSRIs, other triptans, MAOIs, propranolol (Inderal), cimetidine (Tagamet), CAD

Tachycardia, bradycardia, throat tightness, closure

2.5 to 5.0 mg orally every two hours to maximal dosage of 10 mg per 24 hours

Ergot-type medications, SSRIs, other triptans, MAOIs, CAD

IM = intramuscularly; SC = subcutaneously; IV = intravenously; SSRIs = selective serotonin reuptake inhibitors; CAD = coronary artery disease; MAOIs = monoamine oxidase inhibitors .

*— Efficacy = clinical impression of effectiveness on a scale of 1t o 4, with 4 being the most effective .

†— Avoid chronic use because of potential for peripheral vasoconstriction .

‡— Frovatriptan (Frova) and almotriptan (Axert) have been released since the article was researched, but generally offer no significant advantages or disadvantages to the trip-tans listed above. Eletriptan is in development .

note : This table is not all-inclusive in treatment protocols, contraindications or adverse reactions. Physicians should consult current Physician's Desk Reference and other pharmacologic resources before prescribing . 16-18 , 22

Information from references 4 , 16 through 18, and 22 .

Subcutaneously injectable sumatriptan (Imitrex) reaches peak blood concentrations faster than any other migraine-specific medications (in approximately 15 minutes) and has been shown to be effective in 70 to 82 percent of patients. The oral form of rizatriptan (Maxalt) reaches peak concentration in 60 to 90 minutes, compared with two to three hours for most other triptans. The longest half-life of the triptans belongs to naratriptan (Amerge). There is some speculation that this longer half-life will decrease the chance of recurrence headaches. In general, if recurrence occurs with use of the triptans, it occurs within eight to 12 hours and can be relieved with a second dose of the medication.16 , 23

Some triptans have the benefit of non-oral routes of administration. Sumatriptan is available in subcutaneous or intranasal form, while rizatriptan (as Maxalt MLT) is offered in an absorbable wafer. When significant nausea and/or vomiting are part of the migraine syndrome, these choices may be better for the patient. Frovatriptan (Frova) and almotriptan (Axert) are oral triptans approved by the U.S. Food and Drug Administration. These and eletriptan (under development) are reportedly more effective, have fewer adverse reactions, and have a more rapid onset of action than sumatriptan.

Several important principles of migraine management have emerged from clinical trials of migraine-specific treatments. First, patients should try a medication for two to three headache episodes before abandoning that line of therapy. Second, if one triptan is ineffective in a patient, a different triptan should be tried. In addition, in selecting a migraine-specific drug, the characteristics of the drug should be matched with the patient's needs and the usual duration of the headache.17 , 18

Various approaches exist for the management of migraine headaches. In the “step-care” approach, patients with acute migraine attacks are initially treated with the safest, least expensive therapies and progress to the more expensive migraine-specific medications, such as the trip-tans, only when the initial treatment fails.24 In contrast, the “stratified-care” approach assigns treatment based on the severity of migraine-related disability, with the nonspecific therapies used in patients with little or infrequent disability, and the migraine-specific medications used in patients with moderate to severe disability. In a recent randomized trial, the stratified-care approach was found to be superior to the step-care approach.25

Nonpharmacologic Alternatives to Migraine Therapy

Because of the current popularity of complementary and alternative therapies, many patients may first request nonpharmacologic treatment. In their consensus guidelines, the U.S. Headache Consortium reviewed behavioral and physical treatments for migraine headaches. Based on available evidence, it appears that relaxation training, thermal biofeedback combined with relaxation training, electromyographic biofeedback, and cognitive-behavioral therapy may be effective in preventing migraines. Behavioral therapy such as relaxation or biofeedback may be combined with preventive drug therapy to achieve additional clinical improvement. Other modalities, such as acupuncture, hypnosis, transcutaneous electrical nerve stimulation, cervical manipulation, occlusal adjustment, and hyperbaric oxygen, have shown mixed results in reported studies but may be worth trying in patients who want to use medication only as a last resort.

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The Authors

GLEN AUKERMAN, M.D., is professor in the Department of Family Medicine at Ohio State University College of Medicine and Public Health in Columbus. He received his medical degree from Ohio State University College of Medicine. Dr. Aukerman is past president of the Ohio Academy of Family Physicians and the American Academy of Family Physicians. .

DOUG KNUTSON, M.D., is assistant professor in the Department of Family Medicine at Ohio State University. He received his medical degree from Ohio State University College of Medicine and completed a residency in family medicine at Riverside Methodist Hospital in Columbus, Ohio.

WILLIAM F. MISER, M.D., M.A., is associate professor in the Department of Family Medicine at Ohio State University, where he also serves as residency director. Dr. Miser received his medical degree from Ohio State University College of Medicine and completed a residency in family medicine in Augusta, Ga.

Address correspondence to Glen Aukerman, M.D., Department of Family Medicine, Ohio State University College of Medicine and Public Health, 2231 N. High St., Columbus, OH 43201 (e-mail: aukerman-1@medctr.osu.edu ). Reprints are not available from the authors .

The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported .

REFERENCES

1. National Headache Foundation. NHF headache facts. Retrieved April 2002, from: www.headaches.org/factsheet.html . .

2. Rasmussen BK, Jensen R, Schroll M, Olesen J. Epidemiology of headache in a general population—a prevalence study. J Clin Epidemiol. 1991;44:1147–57.

3. Lipton RB, Stewart WF. Migraine in the United States: a review of epidemiology and health care use. Neurology. 1993;43(6 suppl 3):S6–10.

4. Ramadan NM, Silberstein SD, Freitag FG, Gilbert TT, Frishberg BM. Evidence-based guidelines for migraine headache in the primary care setting: pharmacological management for prevention of migraine. U.S. Headache Consortium. Retrieved April 2002, from: www.aan.com/public/practiceguidelines/05.pdf .

5. Hu XH, Markson LE, Lipton RB, Stewart WF, Berger ML. Burden of migraine in the United States: disability and economic costs. Arch Intern Med. 1999;159:813–8.

6. Cady RK. Diagnosis and treatment of migraine. Clin Cornerstone. 1999;1:21–32.

7. Bartleson JD. Treatment of migraine headaches. Mayo Clin Proc. 1999;74:702–8.

8. U.S. Headache Consortium publishes migraine headache treatment guidelines. Retrieved April 2002, from: www.aafp.org/clinical/migraine.

9. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Headache Classification Committee of the International Headache Society. Cephalalgia. 1988;8(Suppl 7):1–96.

10. Moore KL, Noble SL. Drug treatment of migraine: part I. Acute therapy and drug-rebound headache. Am Fam Physician. 1997;56:2039–48.

11. Frishberg BM. The utility of neuroimaging in the evaluation of headache in patients with normal neurologic examinations. Neurology. 1994;44:1191–7.

12. Frishberg BM, Rosenberg JH, Matchar DB, McCrory DC, Pietrzak MP, Rozen TD, et al. U.S. Headache Consortium. Evidence-based guidelines in the primary care setting: neuroimag-ing in patients with nonacute headache. Retrieved April 2002, from: www.aan.com/public/practiceguidelines/02.pdf .

13. Gronseth GS, Greenberg MK. The utility of the electroencephalogram in the evaluation of patients presenting with headache: a review of the literature. Neurology. 1995;45:1263–7.

14. Matchar DB, Young WB, Rosenberg JH, Pietrzak MP, Silberstein SD, Lipton RB, et al. Evidence-based guidelines for migraine headache in the primary care setting: pharmacological management of acute attacks. U.S. Headache Consortium. Retrieved April 2002, from: www.aan.com/public/practiceguidelines/03.pdf .

15. Silberstein SD. Practice parameter: evidence-based guidelines for migraine headache (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2000;55:754–62.

16. Dooley M, Faulds D. Rizatriptan: a review of its efficacy in the management of migraine. Drugs. 1999;58:699–723.

17. Stark S, Spierings EL, McNeal S, Putnam GP, Bolden-Watson CP, O'Quinn S. Naratriptan efficacy in migraineurs who respond poorly to oral sumatriptan. Headache. 2000;40:513–20.

18. Mathew NT, Kailasam J, Gentry P, Chernyshev O. Treatment of nonresponders to oral sumatriptan with zolmitriptan and rizatriptan: a comparative open trial. Headache. 2000;40:464–5.

19. Jones J, Pack S, Chun E. Intramuscular prochlorperazine versus metoclopramide as single-agent therapy for the treatment of acute migraine headache. Am J Emerg Med. 1996;14:262–4.

20. Coppola M, Yealy DM, Leibold RA. Randomized, placebo-controlled evaluation of prochlorperazine versus metoclopramide for emergency department treatment of migraine headache. Ann Emerg Med. 1995;26:541–6.

21. Jackson CM. Effective headache management. Postgrad Med. 1998;104:133–47.

22. Tfelt-Hansen P, Saxena PR, Dahlof C, Pascual J, Lainez M, Henry P, et al. Ergotamine in the acute treatment of migraine: a review and European consensus. Brain. 2000;123(pt 1):9–18.

23. Diener HC, Kaube H, Limmroth V. Antimigraine drugs. J Neurol. 1999;246:515–9.

24. Matchar DB, McCrory DC, Gray RN. Toward evidence-based management of migraine. JAMA. 2000;284:2640–1.

25. Lipton RB, Stewart WF, Stone AM, Lainez MJ, Sawyer JP. Stratified care vs step care strategies for migraine: the Disability in Strategies of Care (DISC) Study: a randomized trial. JAMA. 2000;284:2599–605.

Members of various medical faculties develop articles for “Practical Therapeutics.” This article is one in a series coordinated by the Department of Family Medicine at Ohio State University College of Medicine and Public Health, Columbus. Guest editor of the series is Doug Knutson, M.D.

Copyright © 2002 by the American Academy of Family Physicians.

This content is owned by the AAFP. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP. Contact afpserv@aafp.org for copyright questions and/or permission requests.

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Myer's (Intravenous) Cocktail

Reproduced by permission of Dr. Jonathan Wright

  • Magnesium chloride hexahydrate 20% 2-5 cc
  • Calcium gluconate 10% 1-4 cc
  • Hydroxy-cobalamine 1000 mcg./cc 1 cc
  • Pyridoxine hydrochloride 100 mg./cc 1 cc
  • Dexpanthenol 250 mg./cc 1 cc
  • B-complex 100 1 cc
  • Vitamin C 222 mg./cc 1-30 cc
  • Sterile water to isotonicity: 280-320 mOsm/ml.
  • 1 cc sterile water /cc of calcium gluconate
  • 1 cc calcium gluconate/2 cc magnesium chloride unless anxiety or migraines, then go to 1:1.

  • All nutrients in one syringe and push in over 5-15 minutes through a 25G butterfly.
  • If pain on injection cut with sterile water to 50%
  • Too rapid magnesium can cause severe hypotension.
  • Watch for and correct hypokalemia before administering Myer's cocktail. Suspect hypokalemia in people on diuretics, beta-agonists, corticosteroids, or diarrhea.
  • Measure serum potassium. When in doubt give 25 mEq. of potassium orally at the time of the injection and repeat 4-6 hours later.

These nutritional protocols are for doctors practicing nutritional medicine. They are based on clinical experience and a review of the nutritional literature. They should be correlated with your knowledge and clinical experience and used at your own responsibility.

Offsite Research Articles:

Alternative Medicine Review 2002 Oct;7(5):389-403

This paper presents a rationale for the therapeutic use of intravenous nutrients, reviews the relevant published clinical research, describes the author's clinical experiences, and discusses potential side effects and precautions.

Updated on: Apr. 18, 2013

The Chronicles of Nausea

by Ashli McCall

Beyond Morning Sickness

GERD - Besides a GI cocktail, what else works the same?

ER usually gives me a GI cocktail for bad stomach pain n it helps relieve the pain fast. Is there anything else like it

Responses (3)

A study was done on 3 equal amounts of patients randomly assigned to 1 of 3 groups. These patients had to fit a certain profile and had to have come into the ER for dyspepsia (indigestion) relief. The study was done in the ideal manner. Group 1 received an antacid. Group 2 received an antacid + Donnatal. Group 3 received an antacid + Donnatal + lidocaine (your GI cocktail). All groups received essentially the same relief and no one group stood out as the best. There is no "one size fits all, all of the time". You can read about it at the link below:

http (:) //www (.) ncbi (.) nlm(.) nih (.) gov/pubmed/14585449

Here's an example of someone else getting relief:

More information from Wikipedia, the free encyclopedia:

A gastrointestinal cocktail, known as a GI cocktail, is a generic term for a mixture of liquid antacid, viscous lidocaine, and an anticholinergic primarily used to treat dyspepsia. The GI cocktail may also deceptively mask pain originating from the heart.

There is a wide variety of GI cocktail recipes in use today. A very popular one is a mixture of Maalox, viscous lidocaine, and Donnatal, in equal parts. A mixture of 10-30 ml Mylanta, 10 ml Donnatal and 10 ml viscous lidocaine is known as "The Green Goddess," or "Green Lizard." The efficacy of this mixture for the treatment of dyspepsia is generally considered superior to treatment with only any one of its components, due to their varied mechanisms of relief; however, a recent study (see study above) found that a GI cocktail was no more effective in relieving stomach pain than an antacid alone. The treatment may also provide relief for hiatal hernia patients suffering acute symptoms.

Is there something else to take for acid telex beside viscous lidocaine

What else can i use as a substitute of gi coctail used for gerd .

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Understanding the ‘AIDS Cocktail’

Shortly following the discovery of HIV in 1981, a variety of monotherapy treatments, including the better-known treatment called AZT, were introduced to patients in an effort to slow the virus’s progression. Despite initial successes, these monotherapies proved ineffective due to the virus’s ability to quickly develop resistances to single drug therapies.

In 1995, the combination treatment known as the “AIDS Cocktail” was introduced to people with HIV/AIDS. This type of therapy has often been referred to as the highly active antiretroviral therapy (HAART). It may also be called combination antiretroviral therapy (cART), or simply antiretroviral therapy (ART).

Regardless of its name, dramatic improvements have been seen among people who have used combination treatments since they were first initiated.

People who receive combination therapy have reported decreased viral loads, increased CD4 counts, and increased T-cell counts. The life expectancies of HIV patients have become much closer to general mortality rates since the introduction of antiretroviral therapy. The introduction and ongoing successes of the “AIDS Cocktail” has brought a sense of renewed hope about not only the longevity of an HIV-infected person’s life, but also about his or her overall quality of life.

Combination antiretroviral therapy drug regimen classes

A variety of antiretroviral drug therapies are currently available by prescription. Each drug included in the combination therapy serves a unique purpose. The combination of drugs works to prevent the virus from replicating, and in many cases, can restore the patient’s CD4 and T-cell counts, thereby improving the quality and longevity of life.

The current classes of drugs included in antiretroviral therapies include:

  • Nucleoside Reverse Transcriptase Inhibitors(NRTIs): The HIV virus requires reverse transcriptase (RT) in order to replicate. By offering faulty versions of the building blocks for replication to the viruses, the drug therapy works to block the virus’s ability to replicate.
  • Non-Nucleoside Reverse Transcription Inhibitors (NNRTIs): These inhibitors effectively disable a key protein that HIV requires to replicate.
  • Protease Inhibitors(PIs): This inhibitor disables the protein known as protease, another key building block required by HIV to replicate.
  • Entry/Fusion Inhibitors: Unlike the previously mentioned drug therapies, this inhibitor blocks the virus’s ability to enter the body’s CD4 cells.
  • Integrase Inhibitors: Once HIV has penetrated a CD4 cell, it inserts genetic material into the cells with the assistance of a protein known as integrase. This inhibitor blocks the virus’s ability to complete this crucial replication step.

Current recommended HIV treatment protocols

According to the National Institute of Health, the current recommendations for an initial HIV drug regimen includes three HIV medicines and two or more different drug classes. Typically, this includes: two NRTIs with an INSTI, NNRTI, or PI, with ritonavir or cobicistat as a booster.

The drug regimen recommended for each person should take into consideration potential drug interactions, previous drug-resistance testing, and dosing frequency. Once a regimen is put into place, your ongoing reaction and success levels will be carefully monitored by your doctor. In the event of severe side effects or proven ineffectiveness, alterations to the drug regimen will be recommended.

While antiretroviral treatments are currently recommended for all people diagnosed with HIV, those who are currently pregnant, have previously reported an AIDS-defining illness, have been diagnosed with hepatitis B, and have had a recent CD4 count below 500 are considered priority.

Once an antiretroviral treatment is initiated, it should be maintained indefinitely.

Antiretroviral drug therapies previously relied upon achieving two primary outcomes: the inhibition of the proteins protease and reverse transcriptase. Today, recent approvals for additional HIV treatment options that block the virus’s entry into the body’s CD4 cells and the introduction of the virus’s genetic materials (entry inhibitors and integrase inhibitors) expand the number of combinations available to patients.

  • Antiretroviral drugs used in the treatment of HIV infection. (2016, August 9). Retrieved from http://www.fda.gov/ForPatients/Illness/HIVAIDS/Treatment/ucm118915.htm
  • Attacking AIDS with a ‘cocktail’ therapy: Drug combo sends death plummeting. (1999, July 1). Retrieved from https://aidsinfo.nih.gov/news/493/attacking-aids-with-a-cocktail-therapy--drug-combo-sends-deaths-plummeting
  • Bhaskaran, K., Hamouda, O. & Sannes, M. (2008, July 2). Changes in the risk of death after HIV subconversion compared with mortality in the general population. JAMA, 300(1), 51-59. Retrieved from http://jamanetwork.com/journals/jama/fullarticle/182177
  • Pirrone, V., Thakkar, N., Jacobson, J.M., Wigdahl, B. & Krebs, F.C. (2011, May). Combinatorial approaches to the prevention and treatment of HIV-1 infection. Antimicrobial Agents and Chemotherapy, 55(5), 1831-1842. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088245/
  • Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents. (2016, January 28). Retrieved from https://aidsinfo.nih.gov/guidelines/html/1/adult-and-adolescent-arv-guidelines/10/initiation-of-antiretroviral-therapy
  • Mayo Clinic Staff. (2015, July 21). HIV/AIDS. Retrieved February from http://www.mayoclinic.com/health/hiv-aids/DS00005/DSECTION=treatments-and-drugs.
  • Vogel, M., Schwarze-Zander, C., Wasmuth, J., Spengler, U., Sauerbruch, T. & Rockstroh, J.K. (2010, July). The treatment of patients with HIV. Deutsches Arzteblatt International, 107(28-29), 507-516. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2915483/
  • Where to Start: Choosing an HIV Regimen. (2016, February 24). Retrieved from https://aidsinfo.nih.gov/education-materials/fact-sheets/21/53/what-to-start--choosing-an-hiv-regimen

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The Mito Cocktail Explained

During the last MitoAction monthly teleconference on Friday, March 7, 2008, Saad Dinno, RPh, a compounding pharmacist at Acton Pharmacy and Dr. Virginia Tawa, PharmD, discussed the ingredients which make up the mysterious "Mito Cocktail."

"Mito Cocktail" is the name given to a variety of vitamins and supplements which are commonly used by adults and children who have been diagnosed with mitochondrial disease. While there is no cure for mitochondrial disease, many types of the disease including mitochondrial myopathy, mitochondrial cytopathy, MELAS, PDCD, or Complex I, II, III, and IV are responsive to specific vitamin and supplement therapies. Please, consult with your physician before beginning or altering any medication, vitamin or supplement regimen.

The supplements and vitamins used by Mito patients are often high doses and could require a patient to take up to 50 different pills per day. A compounding pharmacist (find one in your area through the IACP, International Academy of Compounding Pharmacists) can create a "cocktail" in a liquid, capsule or other form that combines the pure powdered form of the prescribed supplements and vitamins. The final medication is usually a much smaller amount than if otherwise taken, and can even be flavored to improve palatability. By avoiding fillers common in over the counter tablets, an individual's allergy or dietary restrictions can be accommodated. The exact compound, including dosage and ingredients, is determined by the patient's physician and differs depending on an individual Mito patient's diagnosis, clinical symptoms, weight. Saad and Virginia discussed the most common ingredients used by compounding pharmacists who specialize in treating mitochondrial disease when putting together the "Mito Cocktail", and offered some advice about use and side effects as well.

Coenzyme Q-10 (Coenzyme Q10, CoQ10, CoQ-10, CoQ, ubiquinone, Q-Gel®), is a fat-soluble vitamin-like substance present in every cell of the body and serves as a coenzyme for several of the key enzymatic steps in the production of energy within the cell. It also functions as an antioxidant protecting against accumulation of harmful free radicals, which is important in its clinical effects. Many patients report increased energy while using Coenzyme Q-10, and thus it is a common "front-line" approach to supporting children and adults with mitochondrial disease. Frequently reported side effects include stomach upset and sleep disturbance, so the pharmacists recommend taking Co Q-10 doses earlier in the day and with food. Therapuetic levels may need time to be established, so patients may not see an immediate beneficial effect. In addition, the excess of the substance that is not used is stored in the fat cells, so proper dosing is important.

Another common therapeutic supplement, L-Carnitine (levocarnitine, CARNITOR®) helps to break fat from the food that we eat into energy. Side effects may include diarrhea, and a fishy odor which may be excreted via the sweat glands. Some patients report decreased fatigue and energy improvements by taking L-Carnitine.

Some B-vitamins are cofactors which participate in important mitochondrial reactions. Most of the B-vitamins have a bitter taste and more palatable if flavored. B-vitamins are water soluble; that is, they are excreted if not used, and the benefit from taking these vitamins should be felt immediately.

Thiamin is a cofactor for the pyruvate dehydrogenase complex, and in some patients has improved lactate and pyruvate levels. Thiamin has also helped some patients by improving their clinical symptoms.

Helpful for some patients with headache and migraine, Riboflavin is another important cofactor that participates in important mitochondrial reactions.

Other B vitamins that may be included in the "Mito Cocktail" include: B3, B6, B12 and folic acid (B9). Many patients find folic acid a beneficial ingredient, as this supplement is key in prevention of anemia and assists with the production and health of new cells.

A normal byproduct of the energy cycle are free radicals. Accumulation of free radicals may be especially harmful to mitochondrial disease patients. The use of antioxidants like Vitamin C (ascorbic acid) and Vitamin E (? tocopherol) can help to reduce free radical accumulation, which in some patients may mean improvements in energy and function.

Other common ingredients in the "Mito Cocktail" may include alpha-lipoic acid (another potent antioxidant), creatine, selenium or succinate.

Again, please work with your doctor to determine the exact ingredients to be used in the compound that will be most beneficial for you. One can see that, like some of the best recipes, the "Mito Cocktail" is created for each individual's unique taste!

© 2008 Mitochondrial Disease Action Committee

The Mito Cocktail is one of

The Mito Cocktail is one of the best things to happen to those with mitochondrial disease. It's an incredibly huge blessing to not have to consume 50+ pills every day. I have a patient that uses it and says it's literaly changed her life, simply by altering her morning routine. I highly recommend looking into this for everyone who suffers from this disease.

Dose Cocktail

It’s like Uno™ for Grown Ups!

Dose Cocktail is a fun party game of cards. It is the sum total of all Dose games in one nice-looking box. Players race to get rid of all of their cards and prevent other players from doing the same. Each card is a pun and can advance the game or make players drink. Since winning isn’t as important as having a good time, players can band together, chaotically try to make one or every person drunk, or simply try to get rid of their cards as soon as possible.

In this set, every Infinite Monkey card is collected, as well as all of the cards in each prior game. A $35 value is now available for merely $19.99.

Suicide/Amitriptyline cocktail

Using tricyclic antidepressants (TCAs) as an euthanasia agent, the amitriptyline cocktail (AC) as shown in this article was first described in the book Guide to a Humane Self-Chosen Death written by Dr. Pieter Admiraal and a committee of medical professionals. |The cocktail was further improved by knowledgeable members of ASM to be more reliable and act faster as well.

The two versions of the cocktail Edit

Version #1: the original Amitriptyline Cocktail Edit

This is the original Amitriptyline Cocktail as documented in the book Guide to a Humane Self-Chosen Death.

Version #2: the improved Amitriptyline Cocktail Edit

The original Amitriptyline Cocktail created by Dr. Admiraal had a few issues:

  • The estimated time to death, 36 hours, was far too much. For many people this parameter would be an issue.
  • We were bothered regarding people who were overweight and how would that impact the potency of the cocktail.

Therefore, after cross-checking our data in several sources like Drugs.com, RxList.com, Merck & Co. and Pubmmed.com, we came to the definite conclusions that:

  • 1. Adding cimetidine, which is a cytochrome p450 inhibitor (see the description for cimetidine in this article), would almost double the amitriptyline blood levels and would potentiate it that much, that it would hasten death by far.
  • 2. Adding midazolam would also act to significantly hasten death due to the drugs' interaction, as confirmed by Dr. Admiraal (he said in his book that adding 300 mg of another strong benzodiazepine would hasten death).
  • 3. In cases of people over 100kg, following the data we gleaned from the sources mentioned above, we understood that increasing the needed amount would ensure death.

This table lists the components of the improved cocktail, depending on body weight:

Possible drug substitutions and changes to the cocktail Edit

  • Amitriptyline can be replaced with the following tricyclic antidepressants: clomipramine, desipramine, dosulepin, doxepin, imipramine, nortriptyline and trimipramine.
  • If one cannot obtain midazolam (Dormicum), one had better use any other short-acting benzodiazepine, like lorazepam or temazepam. Alternatively, one can increase the amount of diazepam (Valium) to 500 mg. The use of two kinds of benzodiazepines would significantly hasten death.
  • Do not use phenobarbital in this cocktail, due to unwanted (mainly unpredictable) drug interactions with the amitriptyline.
  • Cimetidine can be replaced with encainide, flecainide or quinidine. It cannot be replaced with Ranitidine or any other antacid medication: see the description for cimetidine in this article.
  • Other benzodiazepines could be usable too. One of the key parameters is the drug half life (how long the drug acts) which you can look up in the benzodiazepine equivalency table.

Mechanism of action and roles of the drugs Edit

Amitriptyline Edit

Amitriptyline is the lethal component of the cocktail.

Tricyclic antidepressants (TCAs) exert their lethality mainly since they are sodium channel blockers. [1]

Sodium channel blockers decrease the propagation and the magnitude of action potentials in the cardiac sytem. The principal effect of reducing the rate and magnitude of depolarisation by blocking sodium channels, is a decrease in conduction velocity (in atrial and ventricular muscle). The faster a cell depolarises, the more rapid adjacent cells will become depolarised, leading to a more rapid regeneration and transmission of action potentials between cells in the cardiac system. Therefore, blocking sodium channels reduces the velocity of action potential transmission within the heart.

This prolongs the QT interval, promoting phenomena like 'torsade de points' or other ventricular tachycardia, which mean that the ventricular muscle would twitch randomly, rather than contracting in unison, and so the ventricles would fail to pump blood into the arteries and into systemic circulation. If the arrhythmia continues, blood circulation will cease, and death (as in, ventricular fibrillation) will occur in a matter of minutes.

The cardiac impact is rather similar to an overdose of Darvon, since Darvon is a sodium channel blocker as well.

Cimetidine Edit

Cimetidine inhibits some of the group of liver isoenzymes named Cytochrome P450,or in short CYP450, which is responsible for the drug's first phase metabolism. Also see the Wikipedia article for CYP2D6. Tricyclic antidepressants like amitriptyline require liver isoenzyme CYP2D6 (along with others of that group) to be metabolised, so inhibiting this enzyme increases the levels of amitriptyline in the blood.

Cimetidine achieves two goals in the cocktail:

  • it hastens death;
  • it eliminates any possibility of survival and renders the cocktail much more lethal.

Cimetidine is normally used to reduce gastric acidity, as a treatment for heartburn or peptic ulcers. But in the cocktail, this mode of action is not relevant; cimetidine is required because of inhibition of the CYP2D6 liver enzyme and not because of its effects on stomach acid. That is why it is not possible to replace cimetidine with ranitidine, or any other antacid medication that a pharmacy might offer to you as a replacement.

Midazolam and Diazepam Edit

Midazolam (Dormicum) is quick acting and of short duration, while Diazepam (Valium)is slower acting but of long duration; both are powerful sedatives from the benzodiazepine class of drugs. They cause deep sleep before amitriptyline starts to act in overdose. Amitriptyline poisoning would be lethal by itself, but the death it causes would not be peaceful.

How long does the cocktail take? Edit

Since TCAs tend to slow the digestive process and absorption from the intestines, death would occur within 12-24 hours.

Is it recommended to use a plastic bag in addition? Edit

The Amitriptyline Cocktail is reliable by itself, if done right. So, there is no reason to use a plastic bag. A plastic bag requires significant preparation and must be used correctly to be lethal. The main risk of combining both is that instead of focusing on doing one thing right, you will do two methods and both wrong.

Comparison to other methods Edit

Amitriptyline is not a narcotic (thus, not a scheduled substance). This makes mail-ordering this drug far less problematic.Template:Pluspoint stop

The cocktail takes a long time to work: up to 36 hours to work for Dr. Admiraal's version and less time for the new, improved one. This obviously increases the chance to be rescued. Potentially, there is a chance to survive with organ damage if rescued at the wrong moment.

Evidence and medical reports attesting to the efficacy of the AC Edit

Amitriptyline and other TCAs accounted for a very large number of death cases all over the globe (some were suicides and some were "accidents").

According to the book Guide to a Humane Self-Chosen Death, which summarises the decisions and inferences of a Dutch euthanasia group's research committee (which consisted of Dr. Pieter Admiraal, who was a well-known anaesthetist, and 5 other experts in their fields), 6 grams of a tricyclic antidepressant has been proven in toxicity reports to be reliably lethal. The committee deemed that adding as little as 300mg of a benzodiazepine would render the death peaceful as well.

The conclusions mentioned above are also supported by the authors of the euthanasia book Beyond Final Exit (see its chapter "Tricyclic antidepressants: A new look"), all of whom possess medical and/or biochemical expertise.

Now, with the other ingredients in the cocktail that we have suggested here (such as cimetidine and two potent sedatives), it would provide for a much more lethal cocktail, one with a much faster and still peaceful demise.

These references document cases of amitriptyline overdose:

  • One case in the ASM newsgroup, from the year 2008.
  • "Deaths related to amitriptyline toxicity are relatively common and are typically related-to suicidal overdose." Source: Amitriptyline Abuse and Misuse. American Journal of-Forensic Medicine & Pathology. 26(1):86-88, March 2005. Prahlow, Joseph A. MD;-Landrum, Jeffry E. DDS
  • "We report here an autopsy case of a 49-year-old woman with depression who died of-hyperthermia, probably due to amitriptyline intoxication." Source: A fatal case of-hyperthermia due to tricyclic antidepressant intoxication, Legal Medicine, Volume 2,-Issue 3, Pages 152-155 (October 2000)
  • "Between the years 1992-2003 in the UK alone, TCA's were responsible for 2700-overdose related deaths where amitriptyline or another TCA was ingested." Source: click here.
  • A Coroner's jury report (Drug Overdose of Amitriptyline). Source: Verdict of Coroner's - Jury into the Death of K. A. Rogers.
  • "The tricyclic antidepressants amitriptyline and doxepin, the most commonly used-antidepressants in Norway, are also the two leading antidepressants causing death by-intoxication." Source: Death due to overdose of antidepressants: experiences from-Norway Acta Psychiatrica Scandinavica Volume 87 Issue s371 Page 28-32, May 1993

Where to obtain the drugs Edit

So far there no good for sure websites you have to keep looking on your own..

Availability of the drugs Edit

  • Amitriptyline (Elavil) is a widely used drug and easily obtainable from on-line pharmacies. It is not on the controlled substance list and ordering it from the internet is legal in most countries. Amitriptyline is often used off-the-label to prevent migraines and tension headaches, so one can use this as an excuse, should any questions arise. Elavil the brand is no longer available in the USA, but generics may still be available in that country.
  • Cimetidine (Tagamet) is a heartburn and ulcer medication, and is not a controlled substance. In the USA and many other countries it is sold over the counter (OTC), which means that it is available without a prescription. In some European countries, and South Africa, cimetidine requires a prescription, so inhabitants of those countries have to buy it over the Internet.
  • Midazolam (Dormicum) and Diazepam (Valium) are drugs from the benzodiazepine class that are commonly prescribed to treat insomnia and anxiety. One can order them over the internet, but keep in mind that benzodiazepines are controlled substances: thus ordering them over the Internet is a criminal offense in some countries. One can also get a prescription legally from one's doctor: if you complain about insomnia and tell your doctor that OTC sleeping pills are not working for you, then your doctor will most likely prescribe a benzodiazepine. A Dormicum prescription is not easily obtained.

Antiemetic regimen Edit

It is very important to use drugs that prevent vomiting (i.e. antiemetic drugs) before one takes the cocktail. Important warnings:

  • OTC antiemetics for motion sickness (Dramamine, Gravol) will not work well.
  • Do not take more antiemetics, or take them more often. It might cause a serious and painful side effect named EPS (short for extrapyramidal symptoms). Have some diphenhydramine (Benadryl, Dimedrol) ready to treat EPS, should it happen to you.

Also, please read this page carefully.

Is there a specific order in which to take the cocktail? Edit

Yes, there is. Please see the quotation below.

How to repackage the drugs in capsules Edit

To reduce the number of tablets to be swallowed, you can repackage tablets in capsules. Below is a post from Son of the Sun explaining this process regarding the Amitriptyline Cocktail.

Also, please see the article Capsules for more information about this subject.

COCKTAIL

Dictionary entry overview: What does cocktail mean?

The noun COCKTAIL has 2 senses:

1. a short mixed drink

2. an appetizer served as a first course at a meal

Familiarity information: COCKTAIL used as a noun is rare.

Dictionary entry details

A short mixed drink

Nouns denoting foods and drinks

Hypernyms ("cocktail" is a kind of. ):

mixed drink (made of two or more ingredients)

Hyponyms (each of the following is a kind of "cocktail"):

old fashioned (a cocktail made of whiskey and bitters and sugar with fruit slices)

pink lady (a cocktail made of gin and brandy with lemon juice and grenadine shaken with an egg white and ice)

Sazerac (a cocktail made with bourbon with bitters and Pernod and sugar served with lemon peel)

screwdriver (a cocktail made with vodka and orange juice)

sidecar (a cocktail made of orange liqueur with lemon juice and brandy)

sour (a cocktail made of a liquor (especially whiskey or gin) mixed with lemon or lime juice and sugar)

stinger (a cocktail made of made of creme de menthe and brandy)

planter's punch (a cocktail made of rum and lime or lemon juice with sugar and sometimes bitters)

gin and it (a cocktail made of gin and sweet vermouth)

martini (a cocktail made of gin (or vodka) with dry vermouth)

Bloody Mary (a cocktail made with vodka and spicy tomato juice)

bullshot (a cocktail made with vodka and beef bouillon or consomme)

daiquiri; rum cocktail (a cocktail made with rum and lime or lemon juice)

gimlet (a cocktail made of gin or vodka and lime juice)

grasshopper (a cocktail made of creme de menthe and cream (sometimes with creme de cacao))

Harvey Wallbanger (a cocktail made of vodka or gin and orange juice and Galliano)

manhattan (a cocktail made with whiskey and sweet vermouth with a dash of bitters)

margarita (a cocktail made of tequila and triple sec with lime and lemon juice)

White Russian (a cocktail made with vodka, coffee liqueur, and milk or cream)

An appetizer served as a first course at a meal

Nouns denoting foods and drinks

Hypernyms ("cocktail" is a kind of. ):

appetiser; appetizer; starter (food or drink to stimulate the appetite (usually served before a meal or as the first course))

Hyponyms (each of the following is a kind of "cocktail"):

fruit cocktail (a mixture of sliced or diced fruits)

crab cocktail (a cocktail of cold cooked crabmeat and a sauce)

shrimp cocktail (a cocktail of cold cooked shrimp and a sauce)

Injectable Anesthesia

Anesthetics administered by injection are commonly used in laboratory species. Scroll down for dosage tables and dilution instructions for several drugs and combinations of drugs in a variety of species.

Preparation of Anesthetic Mixtures

While injectable drugs are a convenient way to administer anesthesia to rodents in biomedical research, incorrect use of these drugs can lead to adverse events such as over- or under-dosing and post operative infections. Here are some important guidelines that must be followed to insure animals are appropriately anesthetized and recover uneventfully.

The amount of drug administered to each animal is based on its body weight. Each animal needs to be weighed on the day of anesthesia. Mice and rats, especially young, growing animals, can change weight rapidly. A body weight recorded last week may not be accurate today.

Many factors influence how a particular anesthetic drug and dosage will affect an individual animal. Variables such as strain, sex, age, and stress levels can result in variations in anesthetic depth and recovery times. Try a test administration on non-experimental animals prior to using unfamiliar drugs, drug combinations or groups of animals.

Sterile technique must be used in the preparation and administration of injectable drugs. All needles, syringes and containers used to deliver or store drugs must be sterile. The use of non-sterile equipment can result in animal infections and/or illness.

Controlled drugs are regulated by the U.S. Drug Enforcement Administration and must be stored under double lock and key. Appropriate use and disposal records must be maintained.

Injectable Anesthesia for Laboratory Animals

80-120 mg/kg (K):10-16 mg/kg (X) IP (20-40 min. of anesthesia)

80-100 mg/kg (K): 5-10mg/kg (X) IP (20-50 min. of anesthesia)

22-50 mg/kg (K):2.5-10 mg/kg (X) IM (25-40 minutes of anesthesia)

50 mg/kg (K): 5 mg/kg (X): 1 mg/kg (A) IP (30-45 minutes of anesthesia)

35 mg/kg (K): 5 mg/kg (X): 0.75 mg/kg (A) IM (45-75 min. of anesthesia)

Ketamine:Valium - short duration, light anesthesia

5 mg/kg (K): 0.25 mg/kg (V) IV.

Mix equal volumes of ketamine (100 mg/ml) and valium ( 5 mg/ml). Dosage rate: 1 ml per 20 lbs body weight.

Inactin (thiobutabarbital, EMTU)

80-100 mg/kg IP (60-240 min. of anesthesia)

Pentobarbital -variable anesthetic depth; poor analgesia

30-50 mg/kg IP (20-40 min. of anesthesia)

40-50 mg/kg IP (20-60 min. of anesthesia)

240 mg/kg IP (15-45 min. of anesthesia)

Atipamezole (for reversal of Xylazine)

0.1-1.0 mg/kg IM, IP, SQ or IV (dose required depends on dose of xylazine administered)

0.1 mg/kg IM, SQ (decreases respiratory secretions, prevents bradycardia)

For injectable anesthetic guidelines in other species please consult an ARP veterinarian.

Dilutions of Injectable Anesthetic Mixtures for Use in Rodents

Ketamine/Xylazine

* IP = intraperitoneal injection ** WFI = water for injection

***Xylazine in this mixture is at a concentration of 20 mg/ml. Xylazine is available in concentrations of 20 mg/ml and 100 mg/ml.

Ketamine/Xylazine

* IP = intraperitoneal injection ** WFI = water for injection

Xylazine in the calculation above is at a concentration of 20mg/ml. Xylazine is also available at a concentration of 100 mg/ml. If using 100 mg/ml the volume of xylazine would be 0.2 ml with a volume of 1.8 ml of WFI. The volume of ketamine would remain the same.

Ketamine/Xylazine/Acepromazine

* IP = intraperitoneal injection ** WFI = water for injection

Xylazine in the calculation above is at a concentration of 20mg/ml. Xylazine is also available at a concentration of 100 mg/ml. If using 100 mg/ml the volume of xylazine would be 0.1 ml with a volume of 2.7 ml of WFI. The volume of ketamine would remain the same.

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