Side Effects..... - Page 2

Originally posted by: JUHI.HI

mee too...nvr evn heard abt such side effects!!!😕

Originally posted by: JUHI.HI

i googled n found dis...chk..

I little info I think should be considered about this drug Versed ( Midazolam ) that is used for many medical procedures..

I feel that if people were aware of the effects of this drug they would Opt For Another Drug!
Erasing someones memory of what was done to them is wrong!!

There is simply no good or valid reason to ever purposely induce amnesia during a medical procedure. It is only a recent development in medical thinking that amnesia is somehow a "benefit" to the patient.



In fact, many people who use Versed for " IV Sedation,Conscious Sedation" Twilight Sedation, during a procedure are Awake For The Entire Procedure but remember nothing, often Believing They Were "Out" the whole time.


Versed (Midazolam) is an amnestic. It is also commonly used for minor procedures like setting broken bones,colonoscopies,endoscopies, dental procedures like extractions,conscious sedation,twilight sleep, so that patients won't remember pain and discomfort.HOWEVER THAT DOES NOT MEAN THAT THOSE SENSATIONS WILL NOT BE EXPERIENCED!!!!Forgetting does not mean it did not happen!!

A note from an anesthesiologist
I agree that using midazolam alone in painful situations is wrong. I've heard people getting colonoscopies and screaming, and maybe they remember, maybe they don't.


Here is a note from a Dentist Who uses Versed
I've used Versed 1000+ times during oral surgery procedures and I've never had a complaint. It's a miracle drug because it is safe and it causes you to not remember an unpleasant experience. My answer to him is isn't it better to have not experienced the pain than to have forgot it. No wonder you have had no complaints they have no memory of the procedure...

There is a blog about this drug you may find interesting called Versed Busters just type it into any search engine.

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one more article...in case if u r a biology student or a doctor...if guess then u cn undrstnd dis...btw nthing went into my head😆

An evaluation of the adverse effects of general anesthesia requires an understanding of the effect of anesthesia on the brain. Unfortunately, there is no universally accepted definition of when the brain is anesthetized. Obviously, general anesthesia must alter neuronal functions from their normal physiological state in order to produce analgesia with unconsciousness. The brain is susceptible to anesthetic neurotoxicity at the extremes of ages. In the developing brain of the neonate, anesthetics can induce excessive apoptosis, whereas in the aging brain, subtle cognitive dysfunction can persist long after clearance of the drug (Perouansky 2008).

Inactivation of structures in the limbic system, which normally participate in maintaining consciousness, potentiates the response to a general anesthetic (Ma and Leung 2006). Both inhalational and intravenous anesthetics affect the CNS and the cardiorespiratory systems in a dose-related manner. Neuronal inhibition results in a decreasing level of consciousness and depression of the medullary vital centers, which can lead to cardiorespiratory failure.

Effect on cerebral circulation and metabolism. Most of the volatile anesthetic agents depress cerebral metabolism but increase cerebral blood flow to a varying extent. A disturbed coupling between regional cerebral blood flow and metabolic rate of oxygen has been observed in humans at a moderate depth of anesthesia (Kaisti et al 2003). Propofol reduced regional cerebral blood flow and metabolic rate of oxygen comparably. Sevoflurane reduced regional cerebral blood flow less than propofol but reduced regional metabolic rate of oxygen to an extent similar to propofol.

Effect on electrical activity of the brain. In spite of the depression of excitability of neurons, seizure complexes are frequently observed on EEG under anesthesia with enflurane.

Effect of anesthetics on cognitive development in children. Data from animal studies suggest that exposure to anesthetic agents during the period of rapid brain growth produces neuronal apoptosis with possible long-term functional sequelae. There is suggestion of learning disabilities in some retrospective studies of children who have undergone surgical procedures under general anesthesia, but no conclusions can be drawn about the causal relationship. Prospective, randomized clinical trials are underway to answer the question of whether anesthetic use in children poses a risk to their development (Rappaport et al 2011). One trial at Columbia University in New York will study cognitive function of children exposed to anesthetic agents within the first 3 years of life at ages 8 to 15 years and compare them to sibling pairs who did not have exposure to general anesthesia during surgery.

Delirium. Although delirium is reported frequently after general anesthesia, randomized, controlled trials suggest that no significant difference is seen in the incidence of delirium when general anesthesia and regional anesthesia are compared (Bryson and Wyand 2006). The cause of delirium after anesthesia is due to a persistence of the anesthetic agent interacting with certain risk factors, which include the following:

• Preexisting cognitive disorders or brain damage.
• Over 70 years of age.
• Drug addiction.
• Use of concomitant medications, such as narcotics and high doses of corticosteroids.
• Use of anticholinergic premedications such as atropine.
• Surgical procedures associated with high risk of postoperative delirium, such as coronary artery bypass.
• Intraoperative disturbances such as hypoxia, acidosis, and hypoventilation.
• Postoperative disturbances of electrolytes, fever, and sepsis.

Intravenous agents, such as sodium thiopental, have a shorter duration of action and delirium. Ketamine is more likely to induce delirium accompanied by hallucinations and disorientation.

Dreams and hallucinations. Dreams and hallucinations under sedation or anesthesia are well documented, eg, with use of propofol. Sexual hallucinations may be difficult to disprove and may lead to false allegations of sexual molestation (Schneemilch et al 2012).

Seizures. Certain anesthetic agents, like enflurane, are known to induce seizures and have been used to activate epileptic foci during epilepsy surgery. EEG abnormalities following enflurane anesthesia can persist for several days after exposure, and delayed convulsions can occur. Ketamine lowers the threshold for seizures in epileptic patients. Fentanyl, an opioid used for induction of general anesthesia in patients, has been reported to induce myoclonic activity. The following explanations are given for the abnormal motor activity following use of fentanyl (Jain 2011):

• Fentanyl represents myoclonus or clonus due to blocking of cortical inhibitory pathways that allow the lower cerebral structures to express unsuppressed excitability.
• Opioid-induced motor activity represents a form of exaggerated muscle rigidity, which may sometimes resemble seizures.
• Opioid-induced abnormal motor activity represents subcortical seizures, which are unlikely to be detected by surface electrodes.
• In patients with complex partial seizures, fentanyl has been reported to induce cortical seizure activity from the healthy temporal lobe contralateral to the one from which seizures have been shown to arise. Factors that predispose to perioperative seizures are:
• Use of concomitant drugs known to predispose to seizures.
• Oxygen toxicity.
• Discontinuation of antiepileptic medications in the perioperative period.
• Metabolic abnormalities such as hyponatremia, hypocalcemia, and hypoglycemia.
• Hypothermic circulatory arrest for more than 1 hour increases the likelihood of seizures.

Although rare, cases have been reported of abnormal movements resulting from intravenous propofol anesthesia, which can also induce seizures in susceptible patients. Myoclonic movements have been reported during an induction of anesthesia using propofol (Nimmaanrat 2005).

Stroke. Cerebral ischemia may occur during general anesthesia, but perioperative strokes are more likely to occur due to embolic events. Factors that predispose patients to stroke during or after general anesthesia are:

• A history of hypertension and heart disease.
• Hypotension during general anesthesia.
• Advanced age with a history of transient ischemic attacks, marked carotid stenosis, or both.
• Surgical procedures under general anesthesia associated with a high risk of stroke include open heart surgery, thoracoabdominal aortic surgery, and carotid endarterectomy. Nonrandomized studies have shown that local anesthetic is associated with a significant reduction in the odds of stroke in the perioperative period following carotid endarterectomy. General anesthesia using remifentanil conscious sedation in carotid endarterectomy remarkably lowers the risk of intraoperative stroke as it combines advantages of both general anesthesia and local anesthesia with ease of evaluation of neurologic status (Marcucci et al 2011).
• Bilateral visual loss resulting from anesthesia has been reported in association with ischemic optic neuropathy associated with hypotension (Remigio and Wertenbaker 2000).
• Head rotation or hypertension during intubation, which may produce vertebrobasilar ischemia. Vertebral artery dissection can occur due to abnormal neck position under anesthesia.

The effect of anesthetic agents on the ischemic brain has been studied to evaluate the neuroprotective effect. The protective effect of barbiturates is believed to rest on depression of the cerebral metabolic rate.

Cognitive dysfunction and dementia. Some patients suffer transient postoperative decline in cognitive function, but they usually recover spontaneously. In one study, cognitive impairment could be objectively identified at 1 week after surgery with general anesthesia in 40% of patients, regardless of age, and this risk was reduced slightly by the use of loco-regional anesthesia (Pain and Laalou 2009).

There is a concern that inhaled anesthetics may contribute to neurocognitive dysfunction in Alzheimer disease. Animal experimental studies indicate that inhaled anesthetics influence cognition and amyloidogenesis, but the mechanistic relationship remains unclear (Bianchi et al 2008). Whether long-term exposure to halothane can induce dementia has not been established.

Other factors may be involved in cognitive impairment after general anesthesia. A case is described where vitamin B12 deficiency was identified in a patient who developed cognitive impairment after general anesthesia using nitrous oxide, and improvement followed after vitamin B12 replacement (El Otmani et al 2007).

Myelopathy. Myelopathy may occur due to various mechanisms. Ischemia to the spinal cord may occur from prolonged hypotension, cross clamping of the aorta during some procedures, and hyperlordotic (hyperextension) position during surgery. Anterior spinal artery syndrome may occur. Inferior vena cava flow may be obstructed in this position leading to increased venous pressure in the intraspinal veins, which results in venous infarction of the spinal cord. Perioperative spinal cord stroke with paraplegia is rare, and procedures that increase the risk are aortic, lumbar disc, and scoliosis surgery.

Atlantoaxial instability in patients with trauma, cervical osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and Down syndrome places them at high risk for cervical spinal cord injury during intubation and surgical positioning. Subluxation of the atlantoaxial joint with impingement on the cord may lead to quadriplegia.

An analysis of the American Society of Anesthesiologists Closed Claims database revealed that most cervical spinal cord injuries during general anesthesia occurred in the absence of spinal trauma, instability, or airway difficulties; spine procedures or procedures in sitting position, particularly for cervical spondylosis, were the most common cause (Hindman et al 2011).

Peripheral nerve injuries. These can occur during general anesthesia; the various causative and contributing factors are:

• Improper positioning of the patient during lengthy surgical procedures (most common).
• Unusual stretch on the nerves in the limbs during various maneuvers.
• Nerve ischemia due to vascular disturbances and compression.
• Toxic neuropathy due to the effect of drugs.
• Systemic diseases (diabetes mellitus, uremia, and atherosclerosis) predispose to the development of neuropathy in the perioperative period.

Torticollis. Torticollis has been observed following head and neck surgical procedures under general anesthesia and may be due to atlantoaxial rotatory fixation. It can be detected by CT scan and treated successfully (Jayakrishnan and Teasdale 2000).

A retrospective analysis of an intravenous remifentanil and propofol general anesthetic for craniotomy before awake functional brain mapping revealed that 3 out of 98 patients experienced intraoperative seizures (Keifer et al 2005).

Movement disorders.

Prolonged neuromuscular blockade. Various causes for prolonged duration of neuromuscular weakness following anesthesia are:

• Pseudocholinesterase normally hydrolyses acetylcholine as well as muscle relaxants like succinylcholine and mivacurium. Therefore, in inheritable disorders such as pseudocholinesterase deficiency, there is an abnormally prolonged muscle relaxation if succinylcholine and mivacurium are administered as these drugs are not hydrolysed.
• Systemic diseases with hepatic and renal impairment lead to impaired metabolism and excretion of neuromuscular blocking agents and prolong their action.
• Patients with neuromuscular diseases such as myasthenia gravis and Lambert-Eaton syndrome are at risk.
• Patients with amyotrophic lateral sclerosis may show increased response to vecuronium under general anesthesia with sevoflurane.
• Certain drugs such as anticholinesterases and monoamine oxidase inhibitors can decrease the activity of pseudocholinesterase and prolong neuromuscular weakness.

Spastic paraparesis. Nitrous oxide anesthesia has been implicated in the development of myeloneuropathy. The pathomechanism is inactivation of cobalamin, the active form of vitamin B12 essential for methionine synthetase activity in the CNS and the resulting demyelination. Symptoms and signs of B12 deficiency are variable, but severe deficiency may cause serious neurologic disease, such as spastic paraparesis. Nitrous oxide anaesthesia is a particular risk (Walter 2011). In the case of a young man, daily use of nitrous oxide and oxygen mixture as analgesic produced ataxia and walking difficulty due to dorsal column lesions demonstrated by MRI (Doran et al 2004). The patient recovered after discontinuing nitrous oxide inhalation. In another case, recreational use of nitrous oxide led to cervical myelopathy with low serum B12 levels and lesions of cervical dorsal column shown on MRI (Diamond et al 2004). This patient recovered 3 months after discontinuing nitrous oxide and receiving vitamin B12 injections.

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Originally posted by: FieryLioness

haha... never heard of any such side effect ...

i was actually laughing reading abt it...kuchh bhi dikhate hai 😆