The Arlene Berry Case: With 2010 Update

In Memory Of Arlene H. Berry 1958-2000

The implications of the findings herein are so profound that, according to a hospital insider, Health Canada has issued a "gag-order" in an effort to save face (with so many doctors and nurses involved in this unnecessary death), a blatant attempt not only to prevent the media from becoming involved, but also as a means to deny justice. In my opinion the health authorities have also insinuated themselves into a conspiracy, or party accessory (after the fact) to a medical homicide. These political and ministerial thugs, attached to the public purse, including the sinister College of Physicians and Surgeons of Ontario and their corporate counterparts seem to think that they and the physicians they seek to shield are all above the law. Published under a wide variety of titles internationally, the Arlene Berry case stands as a testament to what can only be construed as widespread corruption in Ontario's health-care system. In Memory of Arlene Berry The FACTS In December of 1999, Arlene Berry was sent to Timmins & District Hospital in Timmins, Ontario, where she was diagnosed, according to her physician, with "carcinoma of the left main bronchus with residual cancer of the aorta due to a complete collapse of the left lung". Her family MD, Dr. Edward. H Jordan had been treating her assumptively for what he termed a "suspected bronchitis". It took another doctor to read her X-ray chart, and to order more appropriate testing before anything was done. On or about January 12th of 2000, Arlene Berry was admitted to the Timmins & District Hospital in Timmins, Ontario, where she had a left lung pneumonectomyon January 13th of 2000, under the care of Dr. Claudio de la Rocha, a Cardiovascular and Thoracic Surgeon who immigrated to Canada from Mexico. Following surgery, Arlene Berry was discharged home 5 days later. On or about March 16thof 2000, Arlene Berry returned to Timmins where she underwent follow-up study and testing at the same hospital, consisting of a CT scan, and a mediastinoscopy with mediastinotomy, as part of her post-operative evaluation. What the family had found to be peculiar however, was a dramatic voice change at some point following the mediastinal procedures, suggesting a "partial vocal fold paralysis" thought to have been procedure related. Although she began to regain her voice in the weeks that followed, her voice remained somewhat "whispery" for the remainder of her days. Following that testing, Arlene confided "I don't have AIDS, or brain tumors, or anything like that, but I might have a "cyst", or "infection". A cystis a suitcase for the infectious material inside. Some of them parasites with simulation of stroke related damage in cultured human nerve cells have been reported. Trapped blood (ie. from an old hemorrhage or occipital bleed) can also lead to the growth of cysts. Patients can be asymptomatic even if the cyst is quite large. Arlene Berry was then referred to the Northeastern Ontario Regional Cancer Centre situated at the Laurentian Site, Sudbury, Ontario for consideration of radiation therapy, under the care of Dr. Hugh Prichard, a radiation oncologist. By the end of April 2000, Arlene Berry had completed her post-operative course of radiationtherapy. In light of this treatment, her condition was seen to be stable. She had been scheduled for X-ray follow-up in Sudbury on Tuesday May 30th at 2:30 PM. Following radiation, Arlene Berry developed "flu-like" symptoms suggestive of gastrointestinal illness within two weeks following radiation therapy, at the end of April of 2000. She died on the 24th of May of 2000. Total time lapse 24 days; mean 3 weeks plus, or just under 4 weeks.

I have given careful consideration to Guillain Barre syndrome. This disorder can develop over the course of hours or days, or it may take up to 3 to 4 weeks. Most people reach the stage of greatest weakness within the first 2 weeks after symptoms appear. 66% reach nadir in 2 weeks, 92% in 3 weeks; by definition MUST peak at 4 weeks

According to her Rx scripts, Arlene Berry had been given Amoxicillin for infection. Amoxicillan belongs to a class of penicillin-like drugs, side effects of which include severe nausea and vomiting, including abdominal pain. According to the hospital record Arlene Berry was admitted to the Kirkland and District Hospital on May 23rd of 2000 by Dr. Spiller for "IV fluid and Gravol", evidenced at A-6. According to record, she was given more than IV and Gravol. If not Dr. Spiller, who ordered the 30 mg MS Contin on his watch? From that record it seems clear that either Dr. Spiller lied, or that he was totally oblivious to the administration of Morphine Sulfate evidenced at A-12. According to the same record, she was admitted for "vomiting".

Vomiting is not a diagnosis, but rather a symptom of many causes.

A-5 of the record documents the presenting complaint as "headaches, accompanied by severe stomach pain", and "abdominal pain ongoing for 2 weeks", for which she had been prescribed "antibiotics". Abdominal or stomach pain concurrent with nausea and vomiting points to the abdomen as the source of the problem, which should have been a 'red flag' suggesting the possibility of intestinal obstruction. Abdominal pain can also be the result of "intestinal ischemia". The hallmark of intestinal ischemia is "abdominal pain". OP-53 documents a history of bloody bowel movements when voiding evidenced by "bloody BM's x 4 days" (bloody, black, or tarry stools). Bloody stools may signify bleeding stomach, diverticular bleeding, or intestinal infection. The same record documents "pale-looking and lethargic". Pale skin suggests decreased blood supply to the skin. Blood vessels in the body constrict to conserve blood in the body's core, making you feel cold and your skin go pale. Lethargy and drowsiness are often associated with moderate to severe dehydration, including congestive heart failure. Lethargy may also be caused by the toxic effects of waste products on brain function. According to the record at OP-53 she was "Here 1 week ago for UTI. Last period on 6th of May". Onset of menstrual periodis closely related to onset of migraine headaches, including illness. Case reports cited primarily in women having period in which a blood-soaked tampon may provide an excellent breeding ground for the bacteria and is a significant cause of urinary tract infections. The same record dated May 22nd documents "For 2 weeks had flu, migraines". Flu symptoms — like headache, fever, chills, stomach pain, usually appear anywhere from 1 to 4 days after a person has been exposed to the virus. Flu headache may be caused by swelling of blood vessels in the brain, due to increasing pressure. Headaches from the flu can feel a lot like migraines. Influenza is not the same as a “stomach flu,” This is most likely due to a GI (gastrointestinal) infection—not the flu. Headaches are also common in people with GI trouble. Many different types of bacteria and parasites can also cause GI infections, leading to CNS infection. According to the record at A-6, she returned to the ED (emergency department) the following day, on May 23rd of 2000 "with the very same complaints".

Rapid evolution of illness and patient return within 24-48 hours suggests a severe illness.

The RN who saw her noted that she had been "taking morphine" for pain management, and also that she had recently "stopped" taking the morphine, noting her recent medical history that for "2 weeks" she had the "flu". The same record also documents a question mark (?) with respect to possible morphine allergies, seen at A-5. OP-53 documents a history of Tylenol and Aspirin, including a documented "daughter states takes a lot", suggests a history of drugs that can break the gastric barrier, and damage the gastric mucosa, ie., NSAID's (non-steroidal anti-inflammatory drugs). Aspirin is the drug classically associated with Reye syndrome. According one of her Rx scripts, Arlene Berry had been prescribed sodium phosphate (usually used to treat constipation) while under the care of her oncologist, and sodium dosucate prescribed by her family MD, and to the best of my knowledge kept taking them following her discharge home, until her prescription ran out. She had found the prescribed laxitives to be ineffective and so turned to over the counter laxitive and tap water enemas for what appeared be drug opiate induced dysmotility.

Constipation, fecal impaction and bowel obstruction are also common problems for oncology patients.

Enema would have been contraindicated, especially in patients with fulminant disease, because of the danger of precipitating toxic megacolon or perforation of the colon. Unfortunately, the health care providers who attended to this patient failed miserably to educate or instruct her in helpful ways. What appears to be a referral at A-6 of the medical record, a chart-copy from the admitting physician (Dr. Spiller), directed to the attention of the family physician, Dr. Jordan, documents what I take to be a provisional diagnosis of "vomiting", while the record at N-11 documents "vomiting, lung CA". According to Dr. Jordan, "she had presented to the ED several days before with vomiting and it was thought that she had a UTI", to rule out delay in seeking treatment. According to the hospital record at A-8 "she was given antibiotics and sent home". According to the outpatient record at OP-54, the patient's recent head CT scan showed "NO METASTASIS", and her mediastinoscopy, a surgical procedure to examine the mediastinum inside of the upper chest between and in front of the lungs, were found to be "NEGATIVE". From that record it seems clear that NO clinically detectable metastasis were found. The Health Management Record at A-21 of the record documents the patient's sensory cognitive perceptual pattern as "sedated". Increased sedation is also a serious side effect of many pharma agents, including electrolyte derangements which can mimic sedative intoxication. The record at A-23 documents a "slurred speech" as evidenced by a checkmark in the upper left corner. Speech that is unintelligible, slurred, or whispery, suggests that the various muscles required to form speech are weakened. The record at OP-54 dated May 22nd of 2000 documents a "haggard appearance", including "large blood trace leukocytes", what I take to mean leukocyte estrace, marked by an unusually high number of white blood cells (WBC's). Weakness of facial muscles produces a characteristic haggard appearance, or a deceptively disinterested facial expression. The characteristic appearance of a "haggard" or "mournful" face and drooping eyelids is caused by facial muscle paralysis. A sagging mouth or a crooked smile is a part of the same problem. The Outpatient Record from the hospital dated May 22nd of 2000, seen at OP-54 documents a recent history of "hematuria" (blood in urine) for "three days". The healthcare provider who saw her made a diagnosis of UTI. The same record documents a prescription for Cipro, for treatment of "urinary-tract infection". The belated test result however, what I assume to have been a urology test, or a bacterial culture test, evidenced at OP-55 of the record, later returned a finding of "NO Growth". A negative urine test can also suggest the presence of unusual bacteria or viruses causing symptoms of UTI. The record at OP-54 documents "SEPTRA DS GIVEN BEFORE & CIPRO GIVEN AFTER". The same healthcare provider (whose signature is illegible) also made a notation with respect to the "flu", which was then directed to the attention of the patient's "family MD", namely, Dr. Jordan. Cipro is a broad-spectrum antibiotic indicated in the treatment of a variety of infections, including the flu. Bactrim/Septra is also the antibiotic most frequently associated with drug-induced aseptic meningitis. Certain combinations of medications, such as penicillin and sulfa-based antibiotics can cause the body's immune system to react by over-stimulation, sending white blood cells (called T cells) rampaging through the body destroying its own tissues. This is known as an autoimmune disease and can be triggered following a surgical infection, or by a flu-like illness or a stomach infection. As the immune system fights off the infection, it mistakenly attacks the peripheral nerves. N-9 of the nurses' notes documents a precaution for a "resistant bacteria" ,as evidenced by a check mark in the upper right hand corner of that document, under the subheading for "INFECTION CONTROL PRECAUTIONS". The same precaution is also noted in the upper right hand corner of the record at A-21. There are no further details.

At the time of her admission to the hospital, Arlene Berry's blood pressure was documented at "115/70 bpm, with a pulse of 79 and regular", with signs of "mild diffuse weakness" and "difficulty ambulating", evidenced at A-6. The same record documents a respiratory rate of 18, on admission. The normal adult respiration rate is 12 to 18 breaths per minute. At the time of this assessment, Arlene Berry was found to be "alert and oriented", with "NO Focal deficits".

The emergency department record at A-6, what I take to be Dr. Spiller's physical examination, documents a "soft, non-tender" abdomen, and "no masses", suggestive of a typical admitting physical note to express an overall, normal, negative abdomen. A negative finding can also suggest hypotonia, a disorder that causes low muscle tone that results in muscle weakness. Constipation is more common due to hypotonic gut musculature. Hypotonia is often the presenting sign for many systemic diseases and diseases of the nervous system. The abdominal muscles feel 'soft and doughy'; also a sign of gastropareses in clinical diabetes, which can rapidly progress to intestinal obstruction. On examination, the physician who saw her documented positive bowel sounds, evidenced at A-6. Hyperactive bowel sounds provide the most immediate indication of persistent upper GI bleeding/GI hemorrhage. Gastrointestinal bleeding ALWAYS requires prompt physician evaluation. An increased white blood cell count may indicate an infection. Crampy abdominal pain can suggest accute bleeding. Fatigue, shortness of breath, lethargy and pallor may also be noted. Other findings may include hematemesis, coffee-ground vomitus, bloody stools, Black or tarry stool, rectal passage of bright red clots and jellylike material or melena. Decreased urine output (urinary incontenence), tachycardia, and hypotension accompany blood loss; can also suggest shock from excessive blood loss. Arlene Berry was still neurologically responsive when I saw her following her admission. She was able to reach and use for herself the kidney basin at her bedside table, as she occasioned to vomitmore of the same flu-like "yellowish liquid" that she had done so many times on the days before, and in fact used it for herself in our presence, at which time a cool cloth was provided by the nurses, as evidenced by the record at N-6. The same record documents upwards of "100cc yellowish fluid", what is frank bile, or 'bilious vomit'. The time of that assessment was documented at 1915 hours on May 23, 2000, following Arlene Berry's admission to the Kirkland and District Hospital. The same record documents that the patient had stated she was "very tired", whereupon she was then assisted to bed, as evidenced at N-6. Vomiting is a symptom of many causes. The clinical difference between bilious and non-bilious vomiting (ie, vomiting yellow or green) is critical in distinguishing life threatening abnormalities. The word "bilious" comes from the word cholera. The word cholera is Latin for bilious disease and has come to indicate a severe intestinal infection. People with bowel obstructions may repeatedly vomit yellow, or green colored bile and a history of frequent bilious vomiting in the presence of abdominal pain should have been a 'red flag' suggesting intestinal obstruction, which should have been treated emergently. Arlene Berry also complained of being "cold" and so the nurses provided her with extra blankets, evidenced at N-6. Her very last words were that she was "feeling a little better", also evidenced by that record. A-26 documents a body temperature >37.0 . According to the record at the documented temperature is slightly above 37ºC at approximately 37.8 suggesting a low-grade fever. Pathogenic bacteria grow best at human body temperatures in the 37ºC range. According to the medical record at N-6 Arlene Berry was admitted at 18:45 hours and had spent 75 minutes in the ER, as evidenced at A-3. In all that time, the ED physician, Dr. Spiller, did very little. NO simple blood tests were done or even ordered at that time. It is also clear that no course of action was charted, marked by a clinically evident inability on the part of the ED physician to adequately make a proper evaluation or even make a provisional diagnosis. In fact, Dr. Spiller had no idea what to look for, electing to play the "wait-and-see" game in the face of life threatening indicators. Not only did the patient's family physician fail to attend, NO diagnosis or differential diagnosis was made following the patient's admission at that time, or at all. NO protocols were followed. A-3 of the record, what I take to be the physician's diagnostic chart is a total blank. Again, from that record it seems clear that nothing was entered because nothing was done. The same record was filed out-of-sequence. The emergency record at A-4 was also filed out-of-sequence. Interestingly both of these records were dated using a rubber stamp that is consistent with backdating techniques. The record at A-12, what I take to be physician orders documents a concomitant or concurrent administration of Senokot (laxative), MS Contin (narcotic analgesic), Statex (morphine family), and Gravol (an anticholingeric agent), including IV solution and additives, the most dangerous of which is the MS Contin, a brand name for "Morphine Sulfate". Co-administration of narcotic analgesics such as MS Contin with laxitives, ie. Senokot may have additive central nervous system (CNS) and gastrointestinal (GI) system effects which can increase the risk of severe constipation or paralytic ileus, including CNS depression. "Contin", is a pharmaceutical industry buzzword for "time-release" or "continuous" release. Additionally, Arlene Berry had been given Statex (a narcotic: opioid agonist analgesic, also used to relieve pain) which also belongs to a class of the morphine family. Notably, morphine is contraindicated to sedation, brain tumours, or increased pressure in the head or spinal cord, possible abdominal problems requiring emergency surgery, in patients having a substantially decreased respiratory reserve, "MS" (morphine sulphate) is often confused with 'Magnesium Sulphate'. Magnesium Sulfate is used to treat severe constipation. Overuse of laxitives, or in combination with bisphosphonates or Magnesium Sulfate, or an overdose of magnesium sulphate used to treat severe constipation can lead to hypermagnesemic pseudo-coma, which mimics a central brainstem herniation syndrome. According to the record at A-13, Arlene Berry was given 30 mg (po bid) morphine by nurse McCrank at 2000 hours on May 23rd, the eve of her death in the face of an undiagnosed and undifferentiated condition(s) associated with "abdominal pain". Nurses do not dispense medications to patients without a doctor's order. A judicious dose of morphine on standing order to patients with non-traumatic abdominal pain is usually in the range of 05. mg/kg. The record at N-6 also documents telephone orders received by the hospital from Dr. Jordan at 2030 hours for Stemetil 10mg by IV, 4 times daily for "control of nausea", given by the RN, as further evidenced by the physician's orders seen at A-11. Stemetil suppresses activity in the trigger zones of the vomiting center by "paralyzing the gastrointestinal tract" which governs the vomiting reflex, which can also exacerbate dismotility. A typical single dose of Stemetil for a small woman with low body weight is 5mg. The antiemetic action of Stemetil (prochlorperazine) may "mask the signs and symptoms of drug overdosage from other drugs and may obscure the diagnosis and treatment of other conditions". Increased sedation is a serious side effect of this type of agent. Oversedation results in obtundation, characterized primarily by reduced alertness and hypersomnia. Hypersomnia is defined as a state of sleep in excess of 25% of the expected normal. Further, phenothiazines have even been reported to trigger diabetes in patients with no previous history of diabetes. Morphine and prochlorperazine have a profound impact on bowel motility, often resulting in fecal impaction. The co-administration of a narcotic analgesic and a neuroleptic agent will result in neuroleptanalgesia with drug-induced reduction of oxygen intake, resulting in respiratory depression. Respiratory depression represents the principal negative variable introduced with "conscious sedation" and left unrecognized and untreated, is the cause of panic, including most serious complications. Neurolept-analgesia, also called "conscious sedation" refers to the use of major tranquilisers, ie stemetil/prochlorperazine in conjunction with narcotics such as morphine. Neurolept-analgesia is defined as a state of CNS depression. Notably, my wife had also been given penicillin based medicines and sulfonamides such as Bactrim (Septra DS) and CIPRO (cyproflaxin) on the days before her admission; penicillin and sulfa-based antibiotics can cause the body's immune system to react by overstimulation. Septra DS is an antibacterial agent with a wide spectrum of adversities (difficulty breathing; closing of the throat; swelling of the lips; and unusual bleeding). Cross-reactions between penicillins and sulfa-drugs including sulfonamides are common triggers of drug-induced serum sickness and fixed drug eruptions. Signs and symptoms of overdosage reported with sulfonamides include anorexia, colic, nausea, vomiting, dizziness, headache, fatigue, drowsiness, decreased appetite. Hematuria may also be noted. N-5 of the Nurses' Notes documents "Sudden large queery bloody emesis,reddish brown liquid" at 0255 hours, on May 24th of 2000. Submit, when everything in the intestine slows down, everything in it backs up. N-3 documents an "Suctioned orally thick brownish secretions"at 0320 hours (in the small hours of the morning), suggestive of a more significant backup of intestinal material, i.e., vomiting of fecal matter due to obstruction of the bowel, evidenced by family present as "a large chocolate coloured (gross appearance), odorless, pasty material, looking pretty much like feces". If you are unable to open your bowels due to an obstruction somewhere, then your feces cannot exit your body via the normal route and you can get nauseated and start to vomit fecal matter. This condition requires urgent medical attention and probably surgery. The same record documents "suctioned down ET tube several times for small amount of brownish mucous" (a reddish brown liquid, suggestive of old blood or admixture of blood and gastric content) at 0330 hours, while A-17 documents "being suctioned for moderate amounts of coffee-ground emesis by RN" at 0330 hours on May 24th. Suctioning infers that the patient's airway has become obstructed with secretions or debris. Any negligence of the patient's throat secretions may lead to hypoxia, brain edema and further deterioration in a patient's condition leading to a vicious circle, which if not broken will lead to death. The record at A-5 documents a blood pressure of 115/75 at 17:05 hours on May 23rd that by 18:45 hours had dropped to 100/50 bpm. Marked blood pressure lability with alterations between hypertension and hypotension following paresis suggests an atypical course of GBS. A-20 of the record documents a Glucose of 13.2 H mmol/L (the normal range is 4.1 - 7.8). High blood sugar usually comes on slowly. To convert mmol/l of glucose to mg/dl, multiply by 18. (13.2 x 18) = 237.6 mg/dl. Random Blood Sugar Test (RBS) measures the level of glucose in the body at any point of time. If the level of sugar is between 140 mg/dL and 200 mg/dL, the patient is diagnosed with prediabetes. If the level of sugar exceeds 200 mg/dL, then the patient is diagnosed with diabetes. Glucose levels of 11.1 mmol/l (200 mg/dl) at 2 hours confirms a diagnosis of diabetes. Symptoms of severe high blood sugar include drowsiness and difficulty waking up. A-19 of the record documents an elevated WBC Count of 22.4 H. WBC = Leukocytes. The presence of an elevated WBC count is called Leukocytosis. White cell count is actually 22,400. A normal WBC is 5,000 to 10,000. Normal Adult Range: 3.8-10.8 thous/mcl Optimal Adult Reading: 7.3 WBC leukocytes are the body's primary defense against bacterial infection and also reflect the degree of physiologic stress. WBC's are also elevated with dehydration, and hyperviscosity secondary to dehydration. If the total WBC is high due to a rise in neutrophils and eosinophils, then an allergic, or parasitic process is most likely. An increase in the WBC count (leukocytosis) is also a typical response to noxious stimuli. The record at A-19 documents a Neutrophil count of 92.0 H with an absolute neuts of 20.0 H. Neutrophils, are also known as "segs","PMNs"or "polys"(polymorphonuclears). CSF in bacterial meningitis is typically dominated by the presence of PMNs. PMN’s generally predominate in bacterial infections. Patients with subdural hematoma, metabolic abnormalities, or meningitis may seem to be encephalopathic.

"The presence of polymorphonuclear granulocytes does not rule out the diagnosis of Guillain-Barré syndrome". Eur J Neurol 10(5): 479-86.

Neutrophilia (or neutrophil leukocytosis) is a condition where a person has a high number of neutrophil granulocytesin their blood. Neutrophilia may be due to a number of acute and chronic causes such as infection, inflammation, emotional stimuli, drugs, metabolic hormonal, and endocrine disturbances, including hematologic abnormalities. Wegener's granulomatosis, granulomatous cerebral amebiasis, vasculitis, and heart attack are high on the order of Neutrophilia. Leukocytosis, especially neutrophilia, indicates systemic infection and is rare in the absence of bacterial "superinfection", also called "superbugs" are bacteria, viruses or mixed infection which are resistant to antibiotics. The record at A-19 documents a Lymphocyte count of 2.0 L(low) suggestive of lymphocytopenia in which lymphocytes (T-cells) are reduced with nutritional deficiency, infection, and ascites due to "fluid build-up in the abdomen", and/or an exhausted immune system. If bacterialinfection is present in ascites this may suggest spontaneousbacterial peritonitisin which abdominal pain is a prominent finding. If peritonitis is not treated promptly and effectively multisystem organ failure occurs rapidly. A-19 documents a Red Blood Cell (RBC) Count of 4.30(3.80 - 5.80 is normal), but the HCT (Hematocrit) is very low, with a reduction suggestive of anemia. Anemia is also a prominent cause of dyspnea when the hemoglobin concentration falls below 8-10 g/dl. The same record seen at A-19 documents an HCT count of only 0.361 L (low): HCT is the measurement of the percentage of red blood cells (RBC's) in whole blood. The hematocrit (HCT) is another way of measuring the amount of hemoglobin (Hb), and in this case it is very low. Thus anemia is present when HCT is <>1.0 x 109/L. The monocytes are a type of phagocyte which mature into "macrophages"; they are important germ eating cells. The majority of patients with Guillain-Barré syndrome will have 10 or fewer monocytes. Patients with a low monocyte count have a higher risk of getting sick from an infection, particularly those caused by bacteria. In cancer, or leukemia, the monocytes become elevated. In this case the monocyte count is well below the normal range. A-20 documents an O2SAT (oxygen saturation)- arterial oxygen saturation (SaO2) of 98.9 H, with with a NORMAL reference and an evident run time of 1720 hours, notably several hours after the patient's alleged time of death, following her transfer out to Sudbury on May 24th of 2000. The same record documents an Arterial Ph of 7.437, in the normal range. The time of that assessment is documented at 0400 hours. Hydrogen ion concentration expressed as pH "Power of Hydrogen". A Normal pH is 7.35 - 7.45. Neutral pH is 7. For example, the pH of blood is normally 7.4 and that of muscle is 7.0. pH under 7 is acid; pH over 7 is basic or alkaline. The metabolic pathways of the body require a slightly alkaline environment. Anything below 7.20 is generally considered critical. At 7.0 the heart will stop beating. A-18 of the medical record documents an "inferior ischemia", a sign of reduced oxygen supply to vital organs due to reduced or poor blood flow to the heart. An "inferior ischemia" is the hallmark of "impaired organ perfusion", as it implies that, unless corrected, there may not be enough oxygen in the blood to sustain vital organs. The same record at A-18 documents "Sinus Tachycardia". Sinus tachycardia occurs when the sinus rhythm is faster than 100 beats per minute. The rhythm is similar to normal sinus rhythm with the exception that the RR interval is shorter, less than 0.6 seconds. P waves are present and regular and each P-wave is followed by a QRS complex in a ratio of 1:1. At very rapid rates, the P-waves might become superimposed on the preceding T waves such that the P waves are obscured by T waves. Sinus tachycardia, (>90/min), is seen in over 35% of patients with Guillain-Barré Syndrome, and over 30% suffer from hypertension (Parry, 1993). A-20 documents a Sodium level of 144 (137 - 145) mmo1/L. Sodium is an electrolyte that helps with nerve and muscle function, and also helps to maintain blood pressure. Sodium circulates in the body fluids outside the cells. It is very important for maintaining blood pressure. Sodium is also needed for nerves and muscles to work properly.

CAVEAT: Hyperglycemia can lower the serum sodium concentration by 1.6 mEq/L for each 100 mg/dl, also giving rise to a false test.

A-20 also documents a serum potassium level of 3.4 L at 0400 hours on May 24th of 2000. Low potassium is defined as a potassium level below 3.5 mEq/L. A-20 of the hospital record documents a CK (Creatine Kinase) level of only 40 units per liter (U/L) at 0400 hours. CK is the most sensitive enzyme and in the presence of most diseases, levels can be elevated as much as 50 to 100 times the reference level. In females, total CK should typically be 10 to 79 units per liter (U/L). Metastatic malignant neoplasms cause severe body wasting-cachexia. The hallmark of muscle damage or muscle wasting is elevation of CK concentration.The wasting away of fat and muscle (cachexia) is the most visible hallmark of metastatic cancer. Persons with cancer typically have high CK levels. Notably, Guillain-Barré syndrome does not produce evidence of muscle inflammation such as elevation of the CK. Further, a normal CK (CREATINE KINASE) at the time of the patient's admission would argue favorably against a diagnosis of metastatic CA, at that time. EVIDENCE OF SUBSTANDARD CARE N-10 of the Nurses' Notes document the patient's level of care as "routine", which showed little or NO concern for patient safety. Further, NO close patient monitoring or toxicological screening was done, marked by a complete absence of nursing care plan, as evidenced at A-21 of the medical record. In fact, NO inherent bloodwork was done in a timely manner. NO protocals were ever followed or implemented, in this case. Stemetil is widely distributed into body tissues and fluids. Stemetil undergoes metabolism in the gastric mucosa and on first pass through the liver where it enters the enterohepatic circulation and is excreted chiefly in the feces. Stemetil can also lead to changes in the blood-brain barrier (BBB), allowing an infectious agent to gain entry to the brain and produce lethal central nervous system (CNS = brain and spinal cord) infection. The scientific literature describe two bacterial factors specific to the meningitis pathogen that thwart the normal protective role of the blood-brain barrier, leading to serious infection. Further, sugar solution in IV creates gaps in the blood-brain barrier allowing chemicals to enter. Infected material can block the blood vessels to the brain, and Stemetil can help shuttle it directly into the brain and CNS. Once across the blood-brain barrier, the infection enters neural cells, with resultant disruption in cell functioning, perivascular congestion, hemorrhage, and inflammatory response diffusely affecting gray matter disproportionately to white matter. Blood borne infection in the blood lyse easily. It seems logical to assume that Stemetil would be contraindicated to serious infection for this reason. Stemetil poisoning is marked by oversedation, respiratory depression and hypotension. Stemetil (prochlorperazine) intoxication or poisoning can also cause deep physiologic depression that resembles and can mimic brain death It is also clear that Dr. Jordan sought to eliminate the symptom "nausea", without his attendance, as evidenced by the phone order"for control of nausea" and without any appropriate blood testing, or addressing any possible underlying causes. Further, Dr. Jordan neglected to consider the etiology of the nausea and vomiting as a condition requiring prompt medical intervention. Instead, he elected to give the patient a brain damaging neuroleptic antipsychotic-antiemetic drug without any review of her medical record, and without the benefit of toxicological screening or close monitoring, evidenced at A-21. Clearly, the etiology of the nausea and vomiting had never been determined, as evidenced at A-3. The record at 0020 hours seen at N-6 documents the discovery by duty nurses of the patient's "head against the left side bed rail with her feet under the right side rail". Sensory loss in GBS, if present, takes the form of proprioception (loss of sence of one's own perception of the relative position of neighbouring parts of the body to each other), which is occasionally impaired spontaneously, especially with extreme fatigue. The ED physician, Dr. Mark Spiller was up to assess the patient's condition. Upon examination her eyes were documented as being "sluggish". She was simply repositioned by the nurses, as evidenced by the record at N-6. Her"pupils were dilated at approx. 5 mm" with "very little reaction to light", and far from getting better she was becoming progressively worse, as evidenced by a sense of urgency seen on the record to the attendance of the patient with increased activity evidenced at N-6 between 0030 and 0055 hours, also noted at N-5. Clearly, from that record and apart from running around the room looking busy and repositioning the patient, nothing was done. It seems clear that the ED physician failed to properly assess the patient's condition, which fell far below an acceptable standard of care. Further, to add insult to injury, NO blood-work had yet been done. While the clinical feature of 'fixed dilated pupils' is a valuable clinical sign it does not necessarily mean that the patient has severe brain injury. I assume that Dr. Jordan would have been alerted by phone. He claims to have called in at 0100 hours but nevertheless opted not to change his orders, as evidenced by the "no change in orders" seen at N-5. From that record it is clear that Dr. Jordan elected to alienate and treat the patient over the telephone, unseen, in the face of life threatening indicators, all of them ignored and without ever having reviewed the patient record. Further, between 0200 hours and 0220 hours the patient's blood pressure had risen slightly from 150/72to 162/80, a sign of mounting hypertension such as caused or worsened in response to treatment. The record at A-26documents the time of that assessment as 0220 hours, while N-5 documents the time of the same assessment at 0230 hours, a 10 minute difference. The same record documents a HR (heart rate) in the 160's, what is termed "sinus tachycardia". A-26 documents a blood pressure of 162/80 with an SaO2 of 80% at 0220 hours, followed by a lethal drop in blood pressure to 78/70 by 0235 hours, in which blood pressure rises or falls significantly, a hallmark feature of alternating hypotension and hypertension. CAVEAT: Systolic blood pressure <80 mm HG is a hallmark of haemodynamic instability. The term "hemodynamic instability" is most commonly associated with an abnormal or unstable blood pressure, especially hypotension, or trauma due to clinical insult. The record at A-17 documents a complete cessation of the use of abdominal and accessory muscles, evidenced by a "0 use of acc muscles"; and a "0 use of abd muscles"; the muscles of respiration, accessory muscles and diaphragm are affected, suggestive of respiratory and accessory muscle paralysis (crisis) requiring intubation and mechanical ventilation. Functional abdominal muscles also play a role of in conjunction with the accessory expiratory muscles. The time of that assessement is documented at 0330 hours.

Accessory muscle paralysis will result in apprehension and anxiety.

EVIDENCE OF ALTERED RECORDS There are numerous material deficiencies in the related medical record of Arlene Berry which manifest a complete lack of internal consistency, ranging from out of sequence records, from the physician's Discharge note seen at A-1 and A-2, which is mared by error, inconsistency, omission, and contradiction, to the nurses Triage, to obviously rewritten, altered, and falsified medical records, tailored to obfuscate the truth, seen between N-1and N-3 of the nurses notes, with A-16 and A-17 presenting similarly, including as follows: A-26 of the record documents a BP (blood pressure) of 78/70 at 0235 hours, while N-5 documents a BP of 98/70 at the very same time, suggestive of copious error. A-24 documents a heart rate of 174 bpm at 0330 that is consistent with "trauma", while the Ventilation Record documents a heart rate of only 126 at the very same time, a significant difference. A-4 of the record, what I take to be a Trauma Legend, barely visible in the physician’s notes situated in the lower right hand side of that record, there is an "obliterated" area suggesting a white-out, or perhaps an erasure. From that record it seems clear that relevant information was deliberately withheld, or removed to conceal an event. TRAUMA is defined as any insult to the body, clinical or otherwise. The record at A-6 documents a "history of metastatic lung cancer", while the outpatient record at OP-54 clearly documents "no metastasis"and "mediastinoscopy negative". N-4 and N-5 present with less than half a page of documentation consistent with deliberate omission, such as having rewritten that record for the express purpose of withholding incriminating information. A-16 documents a blood pressure of 163/117 at 0330 hourswhile N-3 documents a blood pressure of 136/85 at the very same time. The same record documents a blood pressure of 121/81 at 0400 hours, while N-2 documents a blood pressure of 112/57 at the very same time. More copious error. N-4 of the record documents that Dr. Jordan was called in at 0225 hours. A-1 of the record documents "I was called in later that night because the patient had become obtunded", while the record at N-2 documents "attempts to pull away to painful stimuli" as late as 0400 hours on May 24th, being one hour and thirty-five minutes later, according to the record. Was it the doctor's belief that Arlene Berry ceased to be a human being after becoming unresponsive following undiagnosed, untreated and/or inappropriately treated conditions? So much so that he decided to write her off? N-10 of the record which documents the patient's bowel routine and urinary elimination pattern for toileting is a complete blank, with the very same information that ought to have been recorded, also omitted at OP-53 of the record. The record at N-5 documents a physician "assessments unchanged" despite the fact that the patient had already gone into respiratory distress, as evidenced by "Cheyne-Stokes" respirations with periods of"apnea"lasting"5-8 seconds". Sleep Apnea means"cessation of breath".It is characterized by repetitive episodes of upper airway obstructionthat occur during sleep, usually associated with a reduction in blood oxygen saturation. Other causes include panic attacks. Low oxygen saturation may be present with advanced respiratory muscle involvement. If proper balance is not restored or corrected, the heart and lungs may fail and the brain will literally begin to suffocate. The record at N-5 documents the respirations as "deep and soaring without constant jaw lift"as early as 0220 hours. A-26 of the record documents "gurgling",and "snoring" and is evidenced in the lower left corner of that record. N-5 of the record documents "family in" at 0250 hours. On seeing the patient, we found her to be propped up in the arms of two nurses, gasping for air, with only a plastic oral airway in her mouth. A reason for this , according to the duty nurse was "to keep the patient from swallowing her tongue". It is also of interest to note that NO attempt was made by either of the doctors to place the patient in the ICU in a timely manner. Weakness of tongue and retropharyngeal muscles causes positional airway obstruction; difficulty with protruding tongue and difficulty swallowing indicate that bulbar involvement is significant, which requires that these patients be placed on ventilators in order to breathe. Snoring, sleep apnea and gasping for breath are part of the same problem. Failure to manage the airway with endotracheal intubation when necessary or in a timely manner is clear evidence of negligence. I had asked the patient twice, in the presence of her foster brother, if she could hear me to wiggle her toes, and indeed she did, not once but twice, to be absolutely certain. An observation made by her foster brother as he gently stroked her right cheek was the seeming appearance of the patient attempting to pull her face forward as though trying to lift her head off the pillow. The inability to lift the head off the pillow by flexing the neck is another danger sign associated with GBS; it frequently develops simultaneously with phrenic nerve (diaphram) weakness. In my opinion, Arlene Berry appeared to be more paralyzed or blunted than anything, with the exception of lower limb joint contractions which rapidly diminished and became hyporeflexic. Her condition was cataleptic-like, characterized by a profound hypnotic state, or psychomotor condition of morbid sleep, such as seen in cataplexy, neurolepsis, sleep paralysis, or narcolepsy. Underlying causes of catalepsy include severe emotional trauma, and emotional shock. Compare: neuroleptanalgesia(conscious sedation)in combination with a severely paralyzed motor function. Although patients with GBS in the setting of preserved consciousness may appear to be completely obtunded, they are technically awake and fully lucid. But he/she may literally not be able to move a muscle in response. The GBS patient only appears to be unresponsive due to a severely paralysed motor function. It has been shown that more than half of the time it is the family and not the physician who first realized that the patient was aware. Stuporand coma are characterized by impairment of the arousal system. In stupor, a person arouses only in response to strong verbalor tactile stimuli, awakens briefly, and then lapses back into a sleeplike state after the stimulation stops. In coma, a person cannot be roused to consciousness. With GBS the patient is conscious but unable to respond due to a severely paralysed motor function. N-3 of the record documents "resp noisy","shallow","Cheyne-stoke"at 0320 hours. Cheyne-stokes breathing is a respiratory pattern that oscillates between hypoventilation and hyperventilation, usually the result of diencephalic insult. It is also seen during sleep in some normal individuals. Noise heard during any part of the respiratory cycle may indicate airway obstruction or alteration in airway patency. Patients with neuromuscular disorders have rapid, shallow breathing secondary to severe muscle weakness, which requires that these patients be placed on ventilators in order to breathe. The record at 0255 hours documents a"sudden large bloody-emesis of reddish brown"or what is known in medical circles as "coffee-ground emesis" ie. dark brown tinged vomit the color and consistency of coffee-grounds, composed of gastric juices and old blood, which can rapidly grow bacteria. Vomit that contains blood may have a red or brownish appearance and is called coffee ground vomiting indicating that it has come from large intestines, suggestive of a slow bleeding source in the upper GI tract. Obstruction below the middle of the small bowel also gives rise to brownish vomit. Gastrointestinal (GI) bleeding due to stress ulceration in GBS is reported in the literature. GI bleeding is considered a potential medical emergency. It involves assessing hemodynamic stability, resuscitating the patient as needed, locating the source of the bleed, and treating the underlying cause. From the record it seems clean that NO emergency measures were taken with respect to GI bleeding and that this medical EMERGENCY event was met by the doctors with complete indifference. The record at N-4 documents "incontinent blood tinged urine"at 0305 hours. Incontinent "tinged urine" is consistent with severe dehydration, often mistaken for hematuria (blood in urine). Incontinence can be the result of hypotonia, or neurogenic bladder. Notably, N-3 of the record documents a "large amount of dilute urine" (polyuria) at 0325 hours, only 20 minutes later. This finding would be inconsistent with hematuria. The record at N-2 documents "Foley draining lge amt dilute urine" at 0425 hours, while N-1 of the record documents "Foley catheter emptied for 1200cc dilute urine" at 0450 hours that is consistent with conditions featuring osmotic diuresis and by diabetes insipidus ("water diabetes") It occurs in association with Na+ Disorders, primarily related to Na negligence due to iatrogenic fluid overload. Na is lowered 1.6meq/L for every 100mg/dl glucose. The central causative mechanism in this case, involves a hyperglycemia-induced osmotic diuresis and resultant dehydration. Polyuria due to excess fluid intake and glucose-induced osmotic diuresis is common in patients with transient hyperglycemia. The hyperglycemia emanates from a commonly identified diabetogenic stressor, such as infection, which precipitates the onset of the syndrome, which in turn produces pseudohyponatremia commonly associated with hyperglycemia. A-15 documents the 24 hour IV fluid balance record, that between 1745 hours and 0200 hours was administered as follows: A-14 documents an " IV gid prn", meaning that fluid and medication rate of administration to be is given by IV as follows: "2/3 and 1/3", being a 3.3 % dextrose and 0.3 % sodium chloride @ the rate of 100 cc/hr, as evidenced at A-15. The same record documents a total Na of 1000 cc TBA, (to be absorbed), documented by nurse Bates at 1745 hours; with a 150 ABS (absorbed) by 1900 hours, documented by nurse Ferguson, shows 150 cc absorbed over a period of 75 minutes; far exceeds the rate of 100 cc/hr. Anything above 100 cc/hr points to "overly rapid infusion". Na 850 cc TBA remaining at 1900 hours documented as ABS (absorbed) by 0200 hours, over a period of 7 hours, resulting in a "surplus" of 150 cc fluid, with an additional 1000 cc TBA, and no further documentation with respect to Na monitoring. The ventillation record at A-16shows a complete absence of information with respect to "Water Refill". Hyponatremia results from a "surplus of water" due to Na negligence.Other evidence of fluid overload as indicated by "ascites" due to fluid build-up in the abdomen. Rapid correction of hyponatremia, even mild hyponatremia, risks neurologic complications (see Fluid and Electrolyte Metabolism:Osmotic demyelination syndrome). Generally, Na should be corrected no faster than 0.5 mEq/L/h. Increase should not exceed 10 mEq/L over the first 24 h. Any identified cause of hyponatremia is treated concurrently. The record at N-6 documents "IV infusing well".There are no further IV related entries on that record, or any other record, either to indicate when or if the IV was discontinued, or to show that the rate of administration was being monitored, suggestive of patient dumping, or abandonment, with deliberate omission by reason of Na negligence. The same record documents the use of a No. 20 "Quick Catheter"; signed by nurses Bates, Ferguson, and McCrank (may or may not be relevant). RN is ultimately responsible for monitoring rate of infusion. The same record documents a "hard" IV site in the "R" (right) hand; clot formation due to irritation, of the vein from solution or medications is the most common cause of a hard IV site. The back of the hand has weaker veins, and is not commonly used for IV antibiotics. Seriously ill patients require accurate fluid balance monitoring because IV fluid also contains the medication(s). Rapid infusion may also lead to overdosage. Circulatory overload can occur if IV is not regulated properly and IV fluids infuse too rapidly for the patient's body to handle. Signs of fluid overload include tachycardia, elevated blood pressure, dyspnea and other signs of respiratory distress. Neuromuscular disease is another well-known cause of dyspnea. Notably, Stemetil 10mg was added to the IV at 2030 hours. The drug is sedating and a potent vasodilator, which also crosses the blood-brain barrier. Patients are usually "volume expanded" prior to its use, often due to negligence, resulting in neurologic derangement. Hyponatremia is diagnosed by measuring serum electrolytes. However, serum Na may be artifactually low when severe hyperglycemia increases osmolality. Water moves out of cells into the ECF. Serum Na concentration falls about 1.6 mEq/L for every 100-mg/dL (5.55-mmol/L) rise in the plasma glucose level above normal. This condition is called translational hyponatremia because no net change in the amount of Na has occurred. The record at N-4 documents the patient's "transfer to ICU in respiratory distress" (sudden breathlessness) at 0320 hours, while record at N-3 documents a "congested oral airway" at the very same time, meaning congestion of the breathing passages. Obstruction of the air passages of the nose, mouth, or throat may also lead to difficulty breathing. Certainly the inability to breathe properly can be alarming, and many persons will immediately react with anxiety, fear, or panic. The record at A-24 documents the mechanical charting of the patient's vital signs that commenced recording at 0315 hours. It is interesting to note that the patient's transfer to the ICU had not yet taken place, and that no prior attempt was made by any of the healthcare providers to place the patient in the ICU prior to that time. It seems clear that the healthcare provider had done too little too late as evidenced by the records at N-9, N-10, N-11, including A-3, and A-21. From the record as a whole, it is also clear that both doctors should have realized at the onset, from the severety of the patient's signs and symptoms that they were faced with a critically ill young woman who was not responding to their questionable treatment. They should ALSO have been acutely aware of the danger. Critically ill patients frequently have multiple physiologic derangements that come from a range of possible sources and occur simultaneously. N-5 of the medical record documents a gurgly respirations as evidenced by a "gurgly resps" at 0220 hours, a sign of constriction suggestive of thoracic trauma (patients are often in shock). The same record documents "deep and soaring and without constant jaw thrust", such as associated with the airway and swollowing difficulty in respiratory compromise. Gurgling is a bubling sound. It usually indicates upper airway obstruction from secretions, emesis, or blood. Gurgling respirations indicate the presence of fluid in the airway, usually blood or vomit, or both. The record at N-4 of the Nurses' Notes documents "incontinent blood tinged urine"at 0305 hours that is consistent with urinary incontinence (leakage of urine) or blood tinged urine if bladder infection is also present. Urinary dysfunction such as incontinence (leaking) of urine is a prominant finding in GBS patients due to autonomic abnormalities. Incontinence is loss of bladder control, and is also a very serious side effect of antipsychotic medications. Further, during episodes of hypokalemic periodic paralyses urinary output is decreased during the attack because water accumulates intracellularly in muscles. Dark, concentrated urine in decreasing amounts (incontinent tinged urine)is also a prominant finding in patients with high blood sugar, including dehydration. A-8 of the related record documents "patient was unconscious with respirations of approximately 30 and laboured", that is consistent with dyspnea- difficult or labored breathing. Dyspnea is breathlessness due to high filling pressures and pulmonary congestion/edema, i.e. shortness of breath, a smothering feeling, inability to get enough air, and suffocation. Breathing may become laboured and difficult; laboured breathing is the hallmark of respiratory distress and respiratory failure due to paralysis of the diaphragm. Dyspnea should always be taken seriously. A-1 documents "plantars upgoing bilaterally". Submit that the plantar reflex is a hallmark of the Babinski sign, a test for signs of disease process in the `motor neurons` of the pyramidal tract. Initial drowsiness, bilateral plantar responses, and quadriparesis, is strong clinical evidence of central involvement consistent with drugs or toxins that affect the basal ganglia, thalmus or brain stem. Babinski's sign is also a prominent finding in Bickerstaff's brainstem encephalitis (BBE), a variant of the Guillain Barre syndrome. Further, "limb weakness in GBS is nearly always bilateral" - (Parry, 1993). The lower limb is often ischemic in diabetes. Fecal impaction as a cause of acute lower limb ischemiais also reported in PubMed. The patient became apparently unresponsive, as evidenced at N-5, and went into respiratory distress, requiring ventilation for which she was transferred into ICU at 0320 hours, according to the record at N-3. The same record documents the time of the patient's intubation by Dr. Jordan at 0325 hours, 5 minutes later. What I take to be the Ventilation Record at A-17 documents the arrival in the ICU of the hospital's ventilatory therapist, Helene Studholme at 0330 hours, after being "called in for patient requiring ventilation". From these records, it is clear that either the ventilatory therapist was not present at the time of the intubation procedure because she did not show up until 5 minutes later, or that the intubation did in fact take place at an earlier time, such as 0320. Notably, the record at A-24 documents a HR (heart rate) of 174 bpm at 0320 hours that is consistent with an "awake intubation", (any suspicion of difficulty intubating, for any reason), marked by panic with "awareness". To illustrate, the Vital Signs Record at A-24 documents a heart rate of 174 bpm at 0330 that is consistent with "trauma", while the Ventilation Record seen at A-16 documents a heart rate of only 126 at the very same time, a significant difference, suggesting that the timeline for that event was in fact altered by the Ventilatory Therapist to obfuscate iatrogenic trauma related injury. The Vital Signs Record is a mechanical record with a run time, while the Ventilation Record is a handwritten account, mared by having been rewritten. Which is more likely to make copious errors or downplay an event by omission or telling lies? There is nothing on record to suggest that anesthesia was or wasn't given to prepare the patient for the intubation procedure. My opinion is that if its not on record it didn't happen. The earliest indication of shock is an increase in heart rate (HR). According to Dr. Jordan "the intubation proceeded uneventfully", while N-2 of the record documents the ET (endotrachial tube) "pulled back 4 cm" at 0425 hours. From that record it seems clear that the endotrachial tube had been malpositioned for almost one full hour before the error was discovered by one of the nurses, as evidenced by the record at N-2; infers negligence on the part of the Dr. Jordan, including failure on his part to identify an incorrectly placed airway in a timely manner. Both myself and the patient's foster brother were present to witness that event. Malpositioning of ET tube can cause airway obstructionand may also result in tissue trauma, andbleeding. When an endotrachial tube is misplaced in the esophagus and misplacement is detected late, a compromiseof the patient's safety can be significant. A-12 of the medical record documents a blood pressure of 163/117 bpm at 03:20 hours that by 03:45 hours had dropped to 85/58, following intubation, with an additional drop to 85/52 bpm by 3:52 hours, over a span of some 7 minutes, as evidenced at N-2 in the Nurses' Notes. A-17 documents "being suctioned for moderate amounts of coffee-ground emesis by RN" at 0330 hours. Gastrointestinal bleeding due to stress ulceration is also an important complication in critically ill patients. GI bleeding is a medical emergency that was basically ignored by the healthcare providers, in this case. Stupor and coma are characterized by impairment of the arousal system. In stupor, a person arouses only in response to strong verbalor tactile stimuli, awakens briefly, and then lapses back into a sleeplike state after the stimulation stops. In coma, a person cannot be roused to consciousness. With GBS the patient is conscious but unable to respond due to a severely paralysed motor function. Besides dangerous cardiac manifestations, neuroendocrine changes are also reported and could induce electrolytes and fluid balance impairments. Polyuria has been observed in a severe case of GBS. Polyuria in GBS is multifactorial and would be partly due to a dysregulation of osmoreceptors. The physician's Lab Work Summary at A-19 documents the charting of a course of Hematology (bloodwork) and Coagulation. The same record documents a Fibrinogen level of 4.67 H (the normal range is 2.00-4.00). Elevated fibrinogen levels induce a state of hypercoagulability. When blood protein is high, CSF usually clots because of the presence of increased fibrinogen. Serum fibrinogen levels in a safe range is <300 mg/dL. The plasma fibrinogen level appears to reflect disease activity in acute Guillain-Barré syndrome and is typically elevated at presentation. In fact, ongoing activity of Guillain-Barré syndrome may be reflected by a persistently elevated fibrinogen level. Acute phase reactant: marker of inflammation Further, elevated levels may also be seen with TRAUMA of any kind. A-19 documents a D-dimer test level of 1000 H (<500)(fibrinogen and d-dimer correlates with thrombotic activity) suggests thrombosis. Thrombosis signifies the formation of blood clotting within vessels of the brain or neck. People who are suffering from a severe infection are more likely to develop dangerous blood clots, but inappropriate combinations of medications or treatment can sometimes be the worst offenders. The Cardiac Index at A-18 documents the patient's ventillation rate at 129 bpm (breaths per minute) at 0417 hours, with heart and breath rate increased. Increased heart and breath rate can suggest clinical insult, such as caused or worsened by medications, resulting in oxygen deprivation. The Cardiac Index documents the patient’s age at "55 years", she was only 41 at the time of her death; can imply negligence, or even patient record swapping. A-19 documents the aPTT= activated Partial Thromboplastin Time, a test used to determine the efficacy of various clotting factors used in the diagnosis of coagulation disorders documents the therapeutic range for heparin therapy at 60-100 seconds (23-35 is the normal). The time of that assessment was documented at 0400 hours. The aPTT is typically elevated in 90% of those with coagulopathy. A-19 documents a "PLT ESTIMATE" - "MOD INCREASE" confirming a moderate increase in platelet aggregation activity (blood platelets sticking together), indicating that blood thinners may be needed to prevent blood clots. The ambulance call report seen at N-7, of the Nurses' Notes documents that the patient was intubated and vented and that she was seen to be "stable", but that she appeared to be "pale, dry and cool". In patients with GBS, the skin may become pale and dry, and sweating may become reduced. Body temperature can also be marred by the effects of drug-induced temperature dysregulation, which can suppress sweating, causing central nervous system impairment, often resulting in an afebrile state. Cool, dry skin can also suggest late sepsis, a prominant finding with iatrogenic neglect. Hemodynamic instability has also been defined more broadly as global or regional perfusion that is not adequate to support normal organ function.This definition recognizes the obligation to insure adequate organ perfusion during the flaccid period in patients with GBS. According to the Nurses' Notes at N-1 of the record the patient was given Gravol 50 mg x 10by paramedics at 0620 hours, while the record at N-7with respect to medications documents "See Nsg Notes". Gravol (dimenhydrinate) is contraindicated in lung disease and has also been reported to "mask the presence of underlying organic abnormalities and/or the toxic effects of other drugs". The record at A-8 and A-9 documents "Medi-Vac team were due to arrive at 0435", while the Ambulance Call Sheet documents "call received at 0620" hours, a significant difference. The record at N-7, documents "pulses X 4 good"; head and neck OK; chest OK; "abdomen OK"; pelvis OK; extremities OK. Following her transfer to Sudbury on May 24th of 2000, Arlene Berry's remains was returned to Kirkland Lake several days after family had been notified of her death via her foster brother acting as a family contact, who was notified by phone. On seeing the deceased vicim, her eyes were "sunken in appearance", with swelling and distortion of the face, eyes, and lips, as was the case, marked by a rash-like redness resembling a sunburn with "blistering" wrinkles in the skin in the area just below the right eye, consistent with a delayed hypersensitivity reaction, or fixed drug-eruption, evidenced by all who attended Arlene Berry's viewing at the Monette Funeral Chapel in Kirkland Lake. It is believed that Arlene Berry's death was deliberately provoked and that her eyes were taken by Drs. Sauvé, and Adegbite at the Sudbury Regional Hospital, upon remote third party consent (foster brother), utilizing deception to obtain that consent, by-passing permission from Arlene Berry's immediate family, ie, her de facto common-law spouse and her children. Only biased clinicians might provide less aggressive scrutiny, withhold medical treatment and influence the family in inappropriate ways such as this. Indeed, the fraudulent taking of the patient's eyes in the manner in which it was done can only be construed as theft. From the information at hand, it seems clear that Drs. Sauve and Adegbite sought to open the way, under misleading conditions (influence of drugs, and metabolic disturbances) to organ donation from brain death. The diagnosis of brain death allows organ donation or withdrawal of life support. These doctors allowed this patient to die to achieve their nefarious ends. Certifying brain death to cover-up medical blunders or to increase organ donations constitutes murder. At a first meeting with the coroner held at the OPP Detachment in Kirkland Lake sometime in July of 2001, Dr. Barry A. McLellan, who was the Regional Supervising Coroner for northeastern Ontario at the time admitted to family that there was "no evidence on record to suggest matastasis", meaning spread of cancer. In fact, there is nothing at all on this record to support a diagnosis of cancer in the first place. For the record, fungal, mycobacterial, parasitic, and indolent bacterial infections heve been known to occasionally mimic cancer. In fact, certain pulmonary infections can mimic pulmonary neoplasms. At a subsequent meeting between family and Dr. McLellan, he provided us with a view of a CT scan that was purportedly done in Sudbury, Ontario at the time Arlene's death on May 24thy of 2000, although I suspect it may have been done following withdrawal of llife support. It shows multiple lesions of undetermined origin. The pathogenesis of these yet undetermined lesions remaines unclear but a metabolic disorder seems the most plausible pathological factor. Based on the patient's belated CBC's, the lesions are consistent with collections of purulent exudates (pus producing bacteria), suggested by an elevated Neutrophil count, and/or pockets of pooled blood, as suggested by an elevated Fibrinogen in the presence of an elevated D-dimer, a hallmark of thrombus formation, ie., blood clots. The enhancement is obviously due to infection, or blood pooling, or both. A-1 of the record also documents "she died several days later with numerous metastatic lesions to her brain". According to her death certificate, Arlene Berry died May 24th of 2000, the very same day she was transferred out to Sudbury. As to the cause of death, according to a Dr. Sauve in Sudbury, she died "meeting brain death criteria". No attempt to diagnose was made at that time, or at all. No pathalogical reason was given for the declaration of brain death. No process of exclusion was undertaken without which a diagnosis of brain-death should never have been considered. No autopsy was performed. No appropriate period of observation and/or trial of therapy was ever undertaken. In fact, Arlene Berry was rushed to her death within five and one-half hours of her departure from Kirkland Lake to Sudbury, some 210 miles away. One might ask how much time did these medical dolts actually spend assessing the patient before pulling the plug on her? Although many conditions can mimic brain death clinically upon examination, without excluding them you will KILL a person by homicide, or criminal negligence, despite the reversibility of brain damage. Brain death is defined as the irreversible cessation of function of the entire brain with three specific criteria: 1) coma, 2) absent brainstem reflexes and 3) apnea. In addition to these clinical criteria, there are important prerequisites: 1) NO intoxication or poisoning, 2) NO core temperature greater than 32 degrees Celsius,3) clinical or neuroimaging evidence of acute central nervous system catastrophe and 4) absence of confounding medical conditions such as severe electrolyte, acid-base, or endocrine disturbances. As a safeguard in determining brain death a number of tests need to be carried out every 6 hours and recorded, the physicians performing this determination must not be part of a transplantation team. In some cases, 48 to 72 hours is required to evaluate brain death and a repeat examination with observation up to an additional 24 hours is sometime needed. The length of time between serial examinations to declare brain death varies marginally from 6 to 72 hours. Notably the Sudbury doctors involved were a part of an organ harvesting and transplantation team. It was Dr. Sauve who, utilizing deception, sought to obtain permission from a remote party to obtain the victim's eyes, without immediate family knowledge or consent. With respect to the initial CT scanhereinbefore mentioned, according to the coroner's expert "in the right occipital region there is a spot that measures less than 1 cm that is consistent in appearance with either a small hemorrhage or perhaps a small metastatic tumor". He could only speculate. NO biopsy was done (a biopsy, is required for obtaining tissue for pathological confirmation of the diagnosis). The solitary lesion is also consistent in appearance with an abscess secondary to an occipital dermoid cyst, or early stage cerebritis during/after capsule formation in the early stage of abscess development. Rupture of a dermoid and leakage of a cyst contents into a ventricle or subarachnoid space may produce an epidymitis or meningitis respectively. Further, capsules can rupture resulting in the formation of multiple abscesses. The bald truth is that localizing signs of brain tumor include a loss of visionon the side of an occipital neoplasm. Compare occipital abscess, or pyogenic brain abscess, usually of bacterial origin. The occipital lobes interpret vision. Brain tumors are more solid/dense and therefore are usually associated with multi-focal deficits; tumors of the occipital lobe usually produce homonymous hemianopia or partial visual field deficits. Had the lesion been a recent tumor, there would have been onset visual misperception in half of one or both visual fields, with visual impairment and subsequent loss of vision with evolution, prior to hospital admission. That did not happen. Know that even multiple brain abscesses may not cause focal deficit to suggest their presence. Non-neoplastic demyelinating processes of the brain with ring enhancing lesions and mass effect on MRI imaging, mimicking malignant brain tumors, are rare phenomena. The radiologic appearance of demyelinating pseudotumors as contrast-enhancing solitary masses that mimic tumor is well documented, ie., "tumor-like" masses of demyelination, or granulocytes that mimic brain tumors (granulocytes, which are cancer killing cells turn black as they die), or infection. Further, with multiple abscesses or infection the meninges typically show a purulent exudate that obscures the sulci making radiographic appearance of microabscesses less visible, hence they are "not well opacified". Morbidity due to a brain abscess generally results from brain herniation due to mass effect, the result of iatrogenic neglect, or substandard care. No autopsy was performed. Further, a family request for a formal inquest was also denied. Dr. McLellan concluded that Arlene Berry had died of natural causes suggestive of metastatic CA of the brain with multiple brain tumors after eliciting what can only be construed as a most questionable opinion from one of his fellow colleagues believed to be associated with the Sunnybrook Health Sciences Centre, where McLellan spearheaded the North Telehealth Network. However, the medical record of Arlene Berry for May 23rd and 24th of 2000, tells a very different story from the opinion postulated. Eleven percent of mass lesions in cancer patients are not metastases; mass lesions that can masquerade as brain metastasis include abscess(20%) and granuloma (less common and mostly associated with mycobacterial or fungal infection). The commonly observed deficits observed in CNS infection include weakness on one side of the body (hemiparesis), impaired speech production (dysphasia), visual field deficits (may or may not be present), and an inability to smoothly coordinate muscle movements, such as during walking (ataxia). Patients with a dioagnosis of primary or metastic brain tumor(s) associated with a CNS event should have a meticulous review of their history for other possible causes. Brain Tumor is often considered in the diagnosis of lesions demonstrated on brain computed tomography (CT) and/or magnetic resonance imaging (MRI). Brain tumors usually show abnormal densities on CT or altered signal intensities on MRI, mass effect, and sometimes contrast enhancement after the intravenous administration of contrast material. Lesions with these features, however, are not always brain tumors and establishing the diagnosis of a brain tumour is not always a straightforward process. Cerebrovascular diseases, demyelinating processes, inflammatory or infectious diseases, and other miscellaneous diseases can show similar imaging findings. Many non-neoplastic neurological diseases can mimic brain neoplasms on neuroimaging or on histological examination, including multiple sclerosis, stroke, pyogenic abscess, toxoplasmosis, tuberculosis, cysticercosis, fungal infections, syphilis, sarcoidosis, Behçet disease, radiation necrosis, venous thrombosis, Guillain Barre syndrome and others. Multiple intracerebral hematomas can also mimic brain metastases. West Nile virus encephalitis mimicking central nervous system metastases from small cell lung cancer is reported in the literature. The investigation and analysis has been ongoing for almost 9 years with everything pointing to possible GBS, with two second-guess possibilities in the differential which can not be ruled out, namely West Nile Virus, or Botulism, in that order. The differential diagnosis can be difficult, because the symptoms mimic those of Guillain-Barre syndrome. Further, fever in WNV apparently does not present in all cases. With GBS, fever is usually absent at onset. Although brain death mimickery is not an acute finding in WNV, it is with the Miller Fisher variant of GBS, a brainstem encephalitis which also mimics brain death. That botulism may also mimic brain death needs always to be kept in mind. Yet, meningitis, encephalitis and Guillain-Barre syndrome remains undeniably the presentation in this case. I have to ask, is there a common denominator here? Meningitis and encephalitis are usually caused by viruses or bacteria. Less commonly, encephalitis can result from a bacterial infection, such as bacterial meningitis, or it may be a complication of other infectious diseases. Guillain-Barré is preceded by a viral or bacterial infection. Viral meningitis is the most common cause of aseptic meningitis, an inflammatory process involving the meninges in which usual bacterial etiologies cannot be identified. Questionable Opinion: The opinionated author (whose signature was erased) perceives himself to be expert in his field. Believed to be a neurosurgeon, he is generally lacking. The bald truth is that specialists in a given field are not always expert in that field. For the record, his opinion remains unsubstantiated. He also failed to provide any evidence whatsoever which might support a finding of metastatic CA of the brain. Further, a paltry CT scan does NOT provide conclusive proof of metastatic brain tumors. For that it takes a biopsy and in this case that was never done. Therefore the true nature of the lesions were never established. Nor does a CT provide conclusive proof of brain death. In fact the author who rendered the opinion suggesting metastatic cancer is pretty much off-the-wall; what one might expect from a "hand-picked" self-interest cash for comment shill, or someone to one equated with a first year medical student who is thus unworthy of belief. View the medical record of Arlene Berry Further, the opinions expressed by the nameless author admits that his opinion "does not take into account all the facts and circumstances surrounding the patient's death", being his disclaimer. Such a disclaimer also raises doubt about the accuracy of the opinion. He bases his opinion on assumption, while ignoring the facts. Obviously he did not take the time to study the patient's medical record. Instead he opted to tailor or lard his report to justify the opinion that was, in his opinion , being sought by Dr. McLellan for the sake of expediency. This infers a blatant attempt by all concerned to obfuscate the truth. A finding of possible meningitis with abscess of the brain and/or multiple intracerebral hematomas would have given more credibility to his opinion. In fact, some of the opinion expressed by the nameless author could also be used to support a finding of meningitis. There is absolutely nothing on record to support a finding of metastatic cancer of the brain, apart from a paltry CT, with no evidence on record to support it. Rapid deterioration is an invariable accompaniment of an untreated condition, in this case, an undiagnosed case of fulminant GBS with overlaping meningitis, in which rapid progress of the disease may actually be displaying a pronounced"blood-brain barrier breach", characterized clinically by "rapid evolution", the result of totally inappropriate treatment, and medications which can breach blood-brain barrier integrity, ie. the drug Stemetil. Breakdown of the blood-brain barrier usually precedes inflammatory demyelination. GBS is often associated with cerebrospinal meningitis and encephalitis. Coma in GBS is rare and is the symptom of cerebrospinal meningitis and encephalitis. The clinical manifestations of this condition included areflexia in the cranial and spinal nerves as well as apnoea. Cisterns may contain pus in cases of meningitis or other inflammatory conditions, such as sarcoid, or demyelination. Any medical professional who, in rendering his opinion as to a cause of death, volunteers his unsolicited opinion as to another doctor’s conduct or standard of care in the face of overwhelming evidence to the contrary, finding in favour of his fellow colleague(s), invites being labeled retrospectively with the most nefarious motives. Although two physicians with experience and expertise must be responsible for the declaration of brain death, and a neurologic condition capable of causing brain death is a mandatory prerequisite to the diagnosis of brain death, there are reports in the literature of conditions that mimic brain death or that provide examples of the mistaken diagnosis of brain death.

The clinical diagnosis of brain death occurred after the patient had received an IV tranquilizing agent and while still under the influence of morphine sulfate, an opiate narcotic.

GBS is one of the few neurological diseases whose clinical manifestations may mimic or appear to be identical to those in brainstem death, illustrating an extreme polyneuropathy.

Canadian standards do not test function of the "entire brain", and there is sound evidence that many individuals who meet the clinical criteria of brain death continue to have some cortical, subcortical, or brain stem function. Many patients diagnosed as brain dead do not have hemodynamic collapse, they have physical findings such as bowel sounds, and are reported to have autonomic reflexes (tachycardia and hypertension) at the time of organ retrieval, suggesting a horrific death. The clinical diagnosis of brain death in this case was made in the presence of metabolic derangements and endocrine abnormalities and constitutes an act of wanton and reckless disregard for human life. There have been many challenges to the several concepts of "brain death" and the means of their diagnosis worldwide (vide infra). Indeed, it seems that there is now an emerging consensus that "brain death" diagnosed by any of the protocols in current use worldwide is "not death." After the diagnosis of brain death, the focus of patient care shifts from interventions aimed at saving the patient's life to interventions aimed at maintaining viability of potentially transplantable organs. Given that current clinical testing does not assess subcortical brain function, ‘whole brain death’ cannot be conclusively identified at the bedside by using clinical criteria, and most certainly not on the basis of a paltry CT scan. The CT is useful only in pretty severe cases, such as head trauma and/or during the few days after an anoxic (lack of oxygen) brain injury and also in cases where there has been a massive stroke. If the question is ischemic injury [brain damage caused by lack of blood/oxygen to part of the brain] you want an MRI and PET. For subsequent evaluation of brain injury, especially brain death, the CT is pretty much useless. Many Ontario physicians actively involved in the identification of brain death, if the truth be known, are unable to identify the requisite diagnostic components of brain death, and/or are unable to apply the criteria correctly. Some physicians will take advantage of the situation to perpetrate a medical murder in order to harvest organs from potential donors, while others will simply declare "brain death" in order to avoid liability for medical wrongdoing. Organ transplantation is premised on professional and public acceptance that the donor is dead and that the cessation of all brain function persists for an appropriate period of observation. The diagnosis of brain death allows organ donation or withdrawal of life support. The diagnosis of brain death is dependent upon the exclusion of certain medical conditions without which the diagnosis of brain-death cannot be considered and influence of medications is one of them. Brain death declaration may be described as an esoteric creation of neurologists and neurosurgeons who are seeking to speed up death for the purposes of an organ transplants. In this case, the harried and hurried physicians did not rely on those esoteric criteria in pronouncing the patient "dead." They simply used the questionable "brain death criteria" (based on a paltry CT after withdrawal of ventillatory support) as a pretext to operate and remove their patient's eyes while she was still very much alive. There are numerous reports of brain death declaration and at least two where the criteria were deliberately misrepresented, or obfuscated in an attempt to retrieve an organ for transplantation, as in this case. Brain death: resolving inconsistencies in the ethical declaration of ... Purpose: The first criteria for the determination of brain death were developed ... two cases were presented where the criteria were deliberately misrepresented in ... www.cja-jca.org/cgi/content/full/50/7/725 More pages from cja-jca.org Status Code 0, or No Code. In my opinion, Arlene Berry's death was premeditated, as evidenced by the physician's documented “Patient Status 0" (code 0), and Dr. McLellan knowingly returned a false finding for which he remains to be held to account. From the facts of this case it seems clear that this moral compass isn't such a straight arrow after all. In a letter to the College of Physicians and Surgeons of Ontario dated November 28, 2000, Dr. Jordan writes "discussed the situation with family members and a decision was made to intubate Ms. Berry", while the Ambulance Call Report seen at N-7 documents an unsigned patient "Status Code 0", or endorsement of a No Code by proxy. This is an order akin to a 'DNR' denying medical intervention, in this case by passing-the-buck together with all the possible blame. Patient condition "Status Code Zero" taken from CMAJ articles, is used to describe a "dead" patient condition. The Yale Law Journal, Vol. 93, No. 2 (Dec., 1983), pp. 362-383, criticizes questionable hospital policies "that resort to third party adjudications in No-Code decision making", and provides insight into the assigning of a "no-code order" instructing personnel "not to attempt resuscitation", as in this case. Looking over the chart it is clear that obtaining a 'no code' status in the face of immune mediated adversities by reason of Dr. Jordan's and Dr. Spiller's failure to recognise and treat an emergency situation accordingly, and by reason of Dr. Jordan's failure to attend in a timely manner was the next essential step for these two negligent physicians in executing Arlene Berry's death in order to avoid liability issues.

The Criminal Code of Canada regards euthanasia, whether passive or active, as culpable homicide, or murder: A culpable homicide is defined as murder "where the person who causes the death of a human being means to cause his death" (s. 229, Criminal Code of Canada). Unless the law has changed in recent years, euthanasia carries a fixed, minimum penalty of 10 years in prison. The 'no code' as evidenced in this case by a "Status Code 0" was ordered by Drs. Jordan, and Spiller, without family knowledge or consent when the patient's condition began to rapidly deteriorate following a whole chain of medical negligence and substandard care that is nothing short of criminal. With the help of Dr. Mark Arthur Spiller (who admitted Arlene Berry to the Kirkland and District Hospital on the evening of May 23rd), a cross-covering physician working the ER with Dr. Jordan on a rotational basis, these two unscrupulous physicians were able to recruit two of their equally unscrupulous Sudbury colleagues to complete their dirty work at arms length. Interestingly, Dr. Spiller had been a local appointed coroner working under Dr. McLellan at the time, and also a classmate of Dr. Stephane Sauve, one of the Sudbury doctors involved in this medical homicide. Although it is clear that Arlene Berry was transferred to Sudbury with ventillatory support, and although Drs. Jordan and Spiller were aware of the need for emergency care and life support, after ordering it, they cancelled it, using the secretive no code (Code 0) endorsement as a pretext for evoking a declaration of death and in fact waited for the patient's death. Within a few hours following her transfer from the Kirkland and District Hospital to the Sudbury Regional Hospital Arlene Berry was declared as having met with 'brain death criteria' , while under the care of Drs. Sauve and Adegbite. Her remains were kept in Sudbury for several days prior to being returned to Kirkland Lake. Withholding life sustaining treatment from an "undiagnosed" patient with concurrent hyperglycemia, hypokalemiaand electrolyte abnormalities in combination with a severely paralysed motor function and who is under the influenceof sedative hypnotic and tranquilizing agents is of questionable legality. Death results from respiratory paralysis and subsequent asphyxiation. Brain death is what happens when ventilator support is discontinued. Turning off a respirator is a form of passive euthanasia that is practiced by doctors with a family's consent. Turn off the respirator and in the natural course of affairs the patient dies from lack of oxygen. To practice euthenasia by withdrawing life support to a critically ill patient is a medical homicide (to kill or destroy by preventing access of air or oxygen). Passive euthenasia involves an allowing of "nature to take its course". Active euthenasia consists of killing someone (to do acts causing death), or by choosing not to act is also an act, which determines the course and the outcome of events. An act of wanton and reckless disregard for human life is an act of criminal negligence, in this case, causing death. In looking over the coroner;s report, was this Dr. McLellan's way of exonerating those responsible for Arlene Berry's death in order to shield the local appointed coroner (working under him at that time) from liability? Or was it just a blatant attempt on his part to shield his fellow colleagues from absolute disgrace? 1. Dr. Sauve sought to open the way to organ donation from brain death under misleading conditions (influence of medications, and metabolic disturbances), further utilizing deception to obtain remote third party consent to harvest my wife's eyes, bypassing permission from the immediate family, namely her defacto spouse and children. 2. Interestingly, Dr. Sauve was a "classmate" of Dr. Mark Spiller, having attended the University of Toronto, Class of '89. Dr. Sauve's name apprears on the Clinical Investigator Inspection List (CLIIL) for Investigational New Drug Studies, and also on the Population Health Research Institute Canada Centre Information list, suggestive of perhaps some hidden agenda, either in the nature of influencing government spending for hospital funding, or some sinister plot involving population control by medical homicide, or both. 3. Suspected of theft of organs for harvesting from a living person by misrepresentation and accessory to medical homicide are: Adegbite, Andrew Babafunso Olanrewaju - Sudbury, ON - (CPSO#54992 ) and Dr. Stephane Jean Sauve - Sudbury (CPSO# 61381); MDs with privileges at the Sudbury Regional Hospital - Laurentian Site. 4. Suspected of criminal negligence causing bodily harm, and liability murder in order to save face are Jordan, Edward Henry - Kirkland Lake, ON (CPSO#61732), and Spiller, Mark Arthur (CPSO#60977); cross-covering physicians working the ER at the Kirkland and District Hospital in Kirkland Lake, ON. In concert with the attending physician, the decision was made by Dr. Jordan to have the patient's senses blunted and prepared for organ harvest. 4. Suspected of conspiracy to conceal an indictable offence(s) and returning a false finding is Dr. Barry Alexander McLellan who so happened to be the Regional Supervising Coroner at the time. Whatsmore, he had been Dr. Spiller's immediate supervisor. A family request for a formal inquest was boldly denied by Dr. McLellan. Interestingly, Dr. McLellan's office was in charge of administering the Human Tissue Gift Act and the Anatomy Act transplants. Dr. McLellan went on to become Ontario's chief coroner and discredited pathologist Charles Smith in order to turn suspicion away from his own faulty findings and sordid immorality. As of September 17, 2007, Dr. McLellan joined Sunnybrook Hospital in Toronto as its new CEO. It is not yet clear whether McLellan stepped down in order to seek refuge among his fellow equally contemptable colleagues at Sunnybrook, or if he was simply given the boot. This case is now a matter of public record. It has been widely reported and publicized through various internet media, Topix forums as well as the Indymedia IMC throughout Canada, the USA, and the UK. The long standing silence of the doctors named herein confirms their active and ongoing concealment, which includes not only secrecy and deception, but also reticence and non-acknowledgment for their part in the Arlene Berry death cover-up. The doctors must have intended the death to occur. It is never per­missible to take any direct action designed to kill a patient. If a doctor deliberately let a patient die who was suffering from a curable illness, the doctor would certainly be to blame for what he had done, just as he would be to blame if he had needlessly killed the patient. Charges against him would then be appropriate. If so, it would be no defense at all for him to insist that he didn't "do anything." He would have done something very serious indeed, for he let his patient die. To allow or hasten a patient's death to cover-up error or negligence, or to obtain organs is reprehensible. It is nothing short of murder since such an act or omission which causes death carries the "intended" consequence of the act or omission, hence, the mens rea or criminal intent. In this case the intent, evidenced by the "Status Code 0" seen at N-7 of the record, is clearly an act of intending to cause the patient's death.

Redress, Information, Analysis 

DaNgeR--DNR!!!

Brain death: resolving inconsistencies in the ethical declaration of death

GUILLAIN BARRE SYNDROME (GBS)

Guillain Barre syndrome | NowPublic News Coverage

Guillain-Barré Overlap syndrome: Signs & Symptoms

Guillain-Barré Syndrome: The Untold Story | NowPublic News

Hidden Agenda: Behind the Scenes

RateMDs.com - Dr. EdwardHenry Jordan Doctor Ratings

Re: Andrew Adegbite, MD.# 54992 Criminal Negligence

Sudbury Regional Hospital - Andrew Adegbite, MD - Topix

Dr. A. B. Adegbite - Sudbury, ON Doctor Ratings | RateMDs.com

Bacterial Gastrointestinal tract (GIT) infections

Infections by Organ System

Medical records for attorneys

Encephalitis: Diagnosis and Treatment