Withdrawing life sustaining treatment from a patient who is under the influence of paralysing agents is of questionable legality. Death results from respiratory paralysis and subsequent asphyxiation.

Prochlorperazine has neuromuscular blocking effects.. intoxication and neuromuscular blockade use are reversible causes of coma that can mimic brain death.

decreased blood pressure, and blood clotting problems could arise in patients especially sensitive or susceptible to changes in histamine levels.

Acquired Neuromuscular Disorders in the Intensive Care Unit

Delayed recovery of consciousness after anaesthesia -- Sinclair ...

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Prolonged neuromuscular blockade  may be  associated with metabolic acidosis,  elevated plasma magnesium concentrations (hypermagnesemia), and female sex   ??? 

- Hypomagnesemia contributes to hypokalemia

Check for involvement of "sulfa" (sulphate) drugs??? = Morphine Sulfate (MS CONTIN):  Symptoms of MS Contin overdose may include:
Cold  skin, flaccid muscles, fluid in the lungs, lowered blood pressure, pinpoint or "dilated" pupils, sleepiness leading to stupor and coma, slowed breathing, slow pulse rate.

Overdosage of morphine is characterized by respiratory depression, with or without concomitant CNS depression. Since respiratory arrest may result either through direct depression of the respiratory center, or as the result of hypoxia, primary attention should be given to the establishment of adequate respiratory exchange through provision of a patent airway and institution of assisted, or controlled, ventilation.

MS Contin - Wikipedia, the free encyclopedia

Morphine overdose can create dilated pupils, drowsiness, coma, low pulse rate, low blood pressure and fluid in the lungs.

Morphine sulfate patient advice including side effects

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Neuromuscular blocking effect of the antibiotic have occurred when it was administered during partial neuromuscular blockade which had been induced by infusion of magnesium sulfate (0.12 or 0.16 g/kg); somethime confused with morphine sulphate, ie. MS.

Because neuromuscular block may paralyze muscles required for breathing, mechanical ventilation should always be available to maintain adequate respiration

Neuromuscular-blocking - Wikipedia, the free encyclopedia it is inappropriate to use the dying equivalent of "conscious sedation" which may be interpreted by courts with a sterile perception of human suffering.

these drugs may cause paralysis of the diaphragm 

causing muscular fasciculations (muscle twitches), clonic twitching?

Patients may have extended paralysis with residual neuromuscular blockade  (apnea and flaccidity) -  not reversing the residual effect could be considered unlawful according to some authors.

Additionally, neuromuscular blockers may facilitate histamine release, which causes hypotension  and tachycardia.

Clinically, neuromuscular block is used as an adjunct to anesthesia to induce paralysis, so that surgery, ie. organ harvesting can be carried out

Neuromuscular-blocking drugs block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. This is accomplished either by acting presynaptically via the inhibition of acetylcholine (ACh) synthesis or release, or by acting postsynaptically at the acetylcholine receptor.

Additionally, these may exhibit cardiovascular effects

The cause of demise is the withdrawal of life support, which leads to loss of circulation and respiration,

effect of hypoperfusion after withdrawal of life support

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1121705

Analgesics - Page 7

Analgesics, Opioid: Information from Answers.com

NO intensive medical therapy WAS OFFERED OR GIVEN

she wiggled her toes in response to my command - suggests the patient was indeed aware of paralysis and verbal stimuli.

Muscle relaxants reduce oxygen consumption

Paralysing agents in current use have no sedative or analgesic actions, although they may mimic this effect from the bedside

Severe disruption of lung architecture, refractory myocardial failure, overwhelming brain injury, and gross metabolic disturbance are the usual causes of rapid death, as exemplified by the case in point - with awareness and discomfort evident in the period after ET tube misplacement

[PDF]

NEJM -- Pharmacologic Paralysis and Withdrawal of Mechanical ...

The 'de facto spouse' wanted "everything done" (aggressive treatment)with ongoing administration of "everything possible" if there was a reasonable chance of salvage but he was never consulted -

Gasping respirations due to neuromuscular blockade are not to be confused with gasping respirations at the end of life

"The cases we describe here are unusual cases in end of life care, since most patients do not enter a prolonged gasping period before dying".
SOURCE: http://jme.bmj.com/cgi/content/full/28/3/164

All neuromuscular blocking agents chemically interrupt neuromuscular transmission resulting in skeletal muscle weakness or paralysis -

Facilitation of mechanical ventilation is the most common reason for subjecting a patient to sustained neuromuscular blockade.

neuromuscular blockade can cause venous thromboembolism, pressureulcers, corneal ulcers, nerve compression syndromes, and muscle atrophy.

sustained neuromuscular blockade has been temporally and anecdotally associated with prolonged skeletal muscle weakness and/or paralysis, although the specific connection to neuromuscular blocking agents is based on histopathologic findings that are difficult to distinguish from the myopathies and axonal polyneuropathies primarily associated with critical illness

Patients receiving neuromuscular blocking agents require constant surveillance, frequent assessment by physical examination, and regularly scheduled evaluations of relevant laboratory studies because most clinical signs and symptoms of acute disease are masked by muscle paralysis.

Using neuromuscular blockade in patients with intracranial injury is controversial. The patient may become paralyzed before he's fully sedated, which can be terrifying for the patient and increase cerebral flow and intracranial pressure. Also, because you can't perform a complete neurologic assessment on a patient receiving NMBs, you may not detect progressive neurologic injury or seizure activity.
http://www.findarticles.com/p/articles/mi_qa3689/is_200011/ai_n8924452

Delayed recovery of consciousness after anaesthesia -- Sinclair ...

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Critical Care Nursing Secrets, 2nd edition

http://intl.elsevierhealth.com/series/secrets/

Hyperglycemia - Diabetes is a direct cause of Hyperglycemia or high blood glucose levels. This condition occurs when there is too much sugar in the blood. Hyperglycemia can lead to more serious complications including Hyperglycemic Hyperosmolar Nonketotic Syndrome and Diabetic Ketoacidosis.

hyperglycemia has been shown to worsen ischemic brain injury

Hypokalaemic periodic paralysis is characterized by attacks of muscle weakness.  Even mild. hypokalemia can lead to cardiac conduction abnormalities. Electrolyte tests are needed.

Hypokalemic periodic paralysis usually involves transient changes in serum potassium concentration while total body stores remain at normal levels. Because our patient had weakness with minimal hypokalemia, the low serum potassium concentration reflects an underlying transcellular disorder rather than a true potassium depletion. Serum potassium concentrations should be normal between paralytic attacks. Electrocardiographic changes can be seen with flattened T waves and prominent U waves during attacks of hypokalemic periodic paralysis.

The most common acquired form of hypokalemic periodic paralysis is thyrotoxic hypokalemic periodic paralysis in which episodes of hypokalemic paralysis occur in the setting of thyrotoxicosis.

Hypokalemic paralysis is a heterogeneous group of disorders characterized by 'diffuse weakness' and hypokalemia. The record AT A-6. documents  MUSKULOSKELATAL EXAM:  Reveals  "mild diffuse weakness".

A common cause of diffuse weakness is critical illness polyneuropathy, an axonal disorder that occurs with sepsis and multiorgan failure.

hypokalemia  

Mayo Clinic Proceedings

Association of Hypertension and Hypokalemia

Serum Chemistry Profile Interpretation

http://www.findarticles.com/p/articles/mi_g2601/is_0007/ai_2601000716

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Dehydration - caused by the depletion or lack of intake of fluids in the body, or by restriction of carbohydrates and fat. Restriction/Starvation, vomiting and laxative abuse are the primary causes in sufferers of Eating Disorders. Symptoms include dizziness, weakness, or darkening of urine. It can lead to kidney failure, heart failure, seizures, brain damage and death.
Links:
Dehydration
Dehydration Defined

Edema - swelling of the soft tissues as a result of excess water accumulation. It is most common in the legs and feet of Compulsive Overeaters and in the abdominal area of Anorexics and/or Bulimics (can be caused by Laxative and Diuretic use).

Paralysis - transient (or temporary) paralysis -- extreme weakness of muscles or not being able to move at all -- Caused by low levels of potassium, and/or the degeneration of nerve cells, in the spinal cord or in the brain, which have been deprived of essential nutrients. Left untreated, periods of paralysis may happen more frequently and more severly, lead to permanent muscle weakness, and even result in death.
Links:
Periodic Paralysis Association

Chronic Fatigue Syndrome - continuous and crippling fatigue related to a weakened immune system.

Dry Skin and Hair, Brittle Hair and Nails, Hair Loss - cause by Vitamin and Mineral deficiencies, malnutrition and dehydration.

Low Blood Pressure, Hypotension (more common in those with Anorexia and/or Bulimia) - cause by lowered body temperature, malnutrition and dehydration. Can cause heart arrythmias, shock or myocardial infarction.
Links:
Low Blood Pressure
Orthostatic Hypotension - sudden drop in blood pressure upon sitting up or standing. Symptoms include dizziness, blurred vision, passing out, heart pounding and headaches.
Links:
Orthostatic Hypotension

High Blood Pressure, Hypertension - elevated blood pressure exceeding 140 over 90. Can cause: blood vessle changes in the back of the eye creating vision impairement; abnormal thickening of the heart muscle; kidney failure; and brain damage.
Links:
Hypertension

Hyperglycemia

Diabetes - high blood sugar as a result of low production of insulin. This can be caused by hormonal imbalances, hyperglycemia, or chronic pancreatitis.
Links:
Type 2 Diabetes
Eating Disorders and Diabetes

Ketoacidosis - high levels of acids that build up in the blood (known as ketones) caused by the body burning fat (instead of sugar and carbohydrates) to get energy. It can be a result of starvation, excessive purging, dehydration, hyperglycemia and/or alcohol abuse (it can also be a result of uncontrolled or untreated diabetes). It can lead to coma and death.
Links:
Diabetic ketoacidosis

Iron Deficiency, Anemia - this makes the oxygen transporting units within the blood useless and can lead to fatigue, shortness of breath, increased infections, and heart palpitations.
Links:
Anemia
Anemia

Kidney Infection and Failure - your kidneys "clean" the poisons from your body, regulate acid concentration and maintain water balance. Vitamin Deficiencies, dehydration, infection and low blood pressure increase the risks of and associated with kidney infection thus making permanent kidney damage and kidney failure more likely.

Bad Circulation, Slowed or Irregular Heartbeat, Arrhythmias, Angina, Heart Attack - There are many factors associated with having an Eating Disorder that can lead to heart problems or a heart attack. Sudden cardiac arrest can cause permanent damage to the heart, or instant death...
electrolyte imbalances (especially potassium deficiency), dehydration, malnutrition, low blood pressure, extreme orthostatic hypotension, abnormally slow heart rate, electrolyte imbalances, and hormonal imbalances call all cause serious problems with the heart, high blood pressure, accumulation of fat deposits around the heart muscle, high cholesterol, decreased exercise due to lack of mobility, diabetes and hormonal imbalances can all lead to serious problems with the heart.
Links:
Eating Disorders and Heart Disease (American Heart Association)

Lowered body temperature - Temperature Sensitivity - caused by loss of healthy insulating layer of fat and lowered blood pressure.

Cramps, bloating, constipation, diarrhea, incontinence - increased or decreased bowel activity.
Also see: dangerous methods

Weakness and Fatigue - caused by generalized poor eating habits, electrolyte imbalances, vitamin and mineral deficiencies, depression, malnutrition, heart problems.

Seizures - the increased risk of seizures in Anorexic and Bulimic individuals may be caused by dehydration, hyperglycemia or ketoacidosis. It is also possible that lesions on the brain caused by long-term malnutrition and lack of oxygen-carrying cells to the brain may play a role. SOME type of antidepressants can increase the risk of seizure and usually carry a warning against prescribing them to people with Eating Disorders, unless the benefits significantly outweigh the risks.
Links:
Anorexia & Seizures

Death caused by any of the following or any combination of the following: heart attack or heart failure; lung collapse; internal bleeding, stroke, kidney failure, liver failure; pancreatitis, gastric rupture, perforated ulcer, depression and suicide.
Links:
In Loving Memory

Please Also See Signs and Symptoms

Muscle Atrophy - wasting away of muscle and decrease in muscle mass due to the body feeding off of itself.
Impaired Neuromuscular Function - due to vitamin and mineral deficiencies (specifically potassium), and malnutrition.
Links:
Muscle Atrophy Defined

Muscle atrophy

The majority of muscle atrophy in the general population results from disuse. People with sedentary jobs and senior citizens with decreased activity can lose muscle tone and develop significant atrophy. This type of atrophy is reversible with vigorous exercise.

Bed-ridden people can undergo significant muscle wasting. Astronauts, free of the gravitational pull of Earth, can develop decreased muscle tone and loss of calcium from their bones following just a few days of weightlessness.

Muscle atrophy resulting from disease rather than disuse is generally one of two types, that resulting from damage to the nerves that supply the muscles, and disease of the muscle itself.

Examples of diseases affecting the nerves that control muscles would be poliomyelitis (polio) , amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease), and Guillain-Barre syndrome .

Electrolyte Imbalances - electrolyte are essential to the production of the body's "natural electicity" that ensures healthy teeth, joints and bones, nerve and muscle impulses, kidneys and heart, blood sugar levels and the delivery of oxygen to the cells.
Links:
The Minerals That Make Up Electrolytes
Electrolyte Imbalance

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The most serious interactions affecting morphine are with those drugs that also cause sedation. The following drugs may lead to dangerous sedation if taken with morphine - phenothiazines such as chlorpromazine (Thorazine), fluphenazine (Prolixin), thioridazine (Mellaril), and prochlorperazine.

Drug Guide: Morphine Overview on Yahoo! Health

Neuroleptanalgesia - a state of central nervous system depression and analgesia usually produced by a combination of a neuroleptic and a narcotic analgesic.

Opoids: Rapid IV injection can cause hypotension

neuroleptanalgesia

Modification of the injection technique, the hypnotic, the analgesic or the neuroleptic partial effect of the drug combinations produces a number of  variations. The principles of the classical type of neuroleptanalgesia, namely the ability to selectively influence the single components of anaesthesia and the predominant use of a strong analgesic must remain unaltered in the definition of a variant.

A variety of  opioids and tranquillizers can be combined to produce neuroleptanalgesia;

Phenothiazines demonstrate a dose-dependent spectrum of activity ranging from anxiolysis to sedation and drowziness. They have virtually no analgesic effects but appear to potentiate the analgesic effects of opioids. Centrally, phenothiazines mediate their effects via dopamine blockade particularly in the reticular formation. Peripherally they block dopamine and adrenergic receptors resulting in vasodilation and hypotension.

antidopaminergic effects in the basal ganglia and forebrain.

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 Metabolic and hormonal responses to neuroleptanalgesia (prochlorperazine and morphine sulphate):

Administration of prochlorperazine and morphine sulphate to oncology patient associated with an increase in  blood glucose,

Respiratory acidosis or alkalosis in patients under the influence of neurolept analgesia may obscure or mimic electroencephalographic abnormalities caused by intracranial disease.

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The patient may have arrested and suffered permanent anoxic injury.

Neuromuscular blocking agents are considered high-alert drugs because misuse can lead to catastrophic injuries or death.

.Neuromuscular Blocking Agents
(Immobilizing Drugs or Paralyties):

Neuromuscular blocking agents inhibit the transmission of nerve impulses at the neuromuscular junction resulting in skeletal muscle paralysis and profound muscular relaxation without loss of consciousness.

BLOCKING THE ACTION

Neuromuscular blockers can be classified as depolarizing ( causes sodium and calcium to flow into the cell. This causes the muscle cell membrane to depolarize and the muscle to contract.) or nondepolarizing, depending on their mechanism of action.

Neuromuscular blockade by some phenothiazine derivatives is reported in PubMed.

Iatrogenic Worsening of Hypokalemia and Neuromuscular Paralysis ...

http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm#Neuromuscular%20Blocking%20Agents(I

Nondepolarizing agents block postsynaptic acetylcholine receptors, preventing impulse transmission and maintaining muscle relaxation and a flaccid paralysis. Neuromuscular blockade with a depolarizing agent begins with a short period of muscle fasciculations followed by muscle paralysis. Patients who are under neuromuscular blockade  may be highly agitated and uncomfortable despite appearing motionless  

Using neuromuscular blockade ( NMB) in patients with intracranial injury is controversial. The patient may become paralyzed before he/she is fully sedated, which can be terrifying for the patient with  increase cerebral blood flow and intracranial pressure. Neuromuscular blockade (NMB) is administered as part of a general anesthetic  NMBs are typically used to facilitate mechanical ventilation.

 Because you can't perform a complete neurologic assessment on a patient receiving NMBs,  you may not detect progressive neurologic injury or seizure activity.

Sedation in the ICU varies widely from producing complete unconsciousness and paralysis to being nursed awake yet comfortable. There are many components to the ideal regimen but key elements include recognition of pain, anxiolysis, amnesia, sleep and muscle relaxation.

Too much or too little sedation and analgesia can cause increased morbidity e.g. oversedation can cause hypotension, prolonged recovery time, delayed weaning, gut ileus, DVT, nausea and immunosuppression, while undersedation can cause hypertension, tachycardia, increased oxygen consumption, myocardial ischaemia, atelectasis, tracheal tube intolerance and infection.

Prochlorperazine  blocks anticholinergic and alpha-adrenergic receptors, the blockade of alpha(1)-adrenergic receptors resulting in sedation, muscle relaxation, and hypotension.

Sedation and Paralysis During Mechanical Ventilation

Effect of spontaneous breathing trial duration on outcome of attempts to discontinue mechanical ventillation…

Opioids can cause apnea prior to pain relief. They promote sedation and analgesia, producing apnea only at high doses.

Search: Stages of analgesia

http://www.petsforum.com/cis-fishnet/JAAS/D078.htm

Brain Failure and Brain Death: Introduction

BD is an iatrogenic state, known only since the development of reanimation and assisted ventilation techniques, which amounts to the death of the person.

Brain cells are extremely sensitive to oxygen deprivation and can begin to die within five minutes after oxygen supply has been cut off. Complete oxygen deprivation for only a few minutes can damage the brain irreversibly. Oxygen deprivation for about seven minutes is sufficient to kill the cerebral cortex.

A brain-dead individual has no electrical activity and no clinical evidence of brain function on neurologic examination (no response to pain, no cranial nerve reflexes (pupillary response (fixed pupils), oculocephalic reflex, corneal reflexes), and no spontaneous respirations). In this case Arlene Berry was breathing spontaneously.

The diagnosis of brain death needs to be made quite rigorously to be certain the condition is truly irreversible. Legal criteria vary from place to place, but generally require neurologic exams by two independent physicians showing complete absence of brain function, and may include two isoelectric (flat-line) EEGs 24 hours apart. In this case, Arlene Berry was declared brain dead within about 5 hours following her transfer to Sudbury.

Brain cells are extremely sensitive to oxygen deprivation. Some brain cells actually start dying less than 5 minutes after their oxygen supply is cut. As a result, brain hypoxia can kill or cause severe brain damage rapidly.

Asphyxiation is the dangerous state that occurs when oxygen does not get from the lungs to the blood as normal.  The absence of oxygen to breathe, suffocation, means no oxygen is getting into the lungs in the first place.

 The heart was still beating because the brain stem continued to function, sending it's regular impulses to the heart muscles-

Heart tissue dies after about 15 minutes of oxygen deprivation, and within an hour most other tissues die as well.

Karakatsanis KG, Tsanakas JN.
A critique on the concept of "brain death".
Issues Law Med. 2002 Fall;18(2):127-41.
"Since the concept of "brain death" was introduced in medical terminology, enough evidence has come to light to show that the concept is based on an unclear and incoherent theory. The "brain death" concept suffers by internal inconsistencies in both the tests-criterion and the criterion-definition relationships. It is also evident that there are residual vegetative functions in "brain dead" patients. Since the content of consciousness is inaccessible in these patients who are in a profound coma, the diagnosis of "brain death" is based on an unproved hypothesis

EEG Alone Cannot Diagnose Brain Death -- Neurotransmitter.net

http://www.sffaith.com/ed/articles/1997/1097ms.htm