|
In Memory Of
Arlene H. Berry
1958-2000
The Arlene Berry Death Coverup: A Liability Murder!
This page is under reconstruction!
"Truth Cannot Live on a Diet of Secrets Withering
Within Entangled Lies" H. Michael Sweeney
Kirkland Lake, ON - JANUARY 2007
Arlene Berry developed flu-like symptoms suggestive of gastrointestinal illness within two weeks following radiation therapy, at the end of April. 2000. She died about about 10 days later. The facts of this case have been taken from the patient's medical record. This is a true story and this case is an ongoing private investigation.
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 initially misdiagnosed her in that he 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 where she had a left lung pneumonectomy on 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 released 5 days later.
CAVEAT: Mexico is a hotbed for amebic infection (amebiasis ). and is believed to be the source of infectious cysts.
Arlene Berry was then referred to the Northeastern Ontario Regional Cancer Centre situated at the Laurentian Site (41 Ramsey Lake Road), 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 a post-operative course of radiation therapy. In light of this treatment her condition was seen to be stable. Postoperative testing results done on March 16th of 2000 in Timmins, were seen to be very encouraging, and from that treatment and testing it seems clear that Arlene Berry had every reason to expect a partial remission, or stable condition.
Following radiation therapy, Arlene Berry had remained quite well until about one week prior to her admission to the Kirkland and District Hospital on the 23rd of May 2000. Over that week she had developed headaches that at times had become increasingly severe. By the second and third week of May of 2000 Arlene Berry was presumed to be suffering from a bout of the "flu" consistent with gastrointestinal illness. The flu is not the only condition starting with flu-like symptoms. Her constilation of symptoms were that of a flu-like illness , marked by general malaise , loss of appetite, nausea, vomiting, and stomach pain accompanied by weakness (tired feeling), chills, and a low grade fever with possible evidence of brain involvement, indicated by lethargy and migraine headaches. One theory of the cause of migraine is a central nervous system (CNS) disorder. The CNS consists of the brain and spinal cord. In migraine, various stimuli may cause a series of neurologic and biochemical events which affect the brain's vascular system. Migraine headaches happen when blood vessels in your head open too wide or close too tight. Vascular headaches are usually throbbing in character, and physical exertion increases the pain. Included under the classification of vascular headaches are migraine headaches, cluster headaches, and toxic headaches. All involve dilation, or swelling of the blood vessels in the head and scalp. While vascular changes are evident during a migraine, the cause of the headache is neurologic, not vascular. Headache predominantly occurs in women. Headaches are also associated with transient ischemic attacks (TIAs), sometimes called "mini-strokes," which result from a temporary lack of blood supply to the brain.
Migraine Cause (Pictures, Images, Photos ...
A severe headache is a common but not invariable accompaniment of intracranial causes of nausea and vomiting, but may also be caused by bacteria or a virus. Nausea and vomiting occur in many disorders. If nausea and vomiting are not controlled in the patient with cancer, the result can be serious metabolic problems such as disturbances in fluid and electrolyte balance and nutritional status.
A-5 of the record documents the presenting complaint as "headaches, accompanied by severe stomache pain", and "abdominal pain ongoing for 2 weeks", for which she was prescribed "antibiotics". The RN who saw her noted that she had also been "taking morphine" for pain management, namely MS Contin, a narcotic analgesic, and also that she had recently "stopped" taking the morphine, noting her recent medical history that for "2 weeks" she had the "flu". The record also documents a question mark (?) with respect to possible morphine allergies. At no time did any of the healthcare providers take time to consider any possible effects associated with withdrawal from opiates. For the two-week period prior to her hospital admission her headaches were accompanied by flu-like symptoms of nausea, vomiting and drowsiness that were thought to be associated with a bout of the "flu", suggestive of a more cephalad (proceeding toward the head) level of infection, or spinal infection which predisposed this patient to paralysis.
The most serious interactions affecting morphine are with those drugs that also cause sedation. The drugs may lead to dangerous sedation if taken with morphine include PHENOTHIAZINES and their derivatives. Stemetil (prochlorperazine) is a piperazine phenothiazine derivative.
According to family the reason that Arlene had "stopped taking the morphine" was due to increasing severity of "constipation", requiring extra laxative and tap water douches to assist with stool evacuation, and also due to dizziness, marked by a sense of uneasiness progressing to unsteadiness, or lack of motor coordination.
According to the patient's Rx List, she had been given sodium phosphate while under the care of her oncologist. Sodium biphosphate and sodium phosphate is used to treat constipation. No follow up was ever done by the patient's family physician, although there is evidence that he was notified at the end of April of 2000 that Arlene had completed her course of radiation therapy. I assume that Dr. Jordan would also have been forwarded a copy of the patient's medical record documenting her most recent treatment, together with the patient's drug regimen at the time he was notified.
Morphine has many side effects. The most dangerous is respiratory depression. Adversities to morphine causes sedation effect, but usually without loss of consciousness. In fragile patients, as the respiratory rate decreases, the patient becomes increasingly sedated.
There is nothing on the record to suggest that this patient had been examined for her stomach pain, either for constipation or possible bowel blockage associated with the morphine. People with bowel obstructions may repeatedly vomit yellow or green colored bile, and may have a distended (swollen, uncomfortable) abdomen. Stomach pain is also a prominent finding associated with dehydration , including constipation.
Straining to evacuate the bowel produces pressure on all of the abdominal wall, forcing the development of hernias, varicose veins (due to pressure on the long veins of the legs), hiatus hernia (upward pressure forcing the stomach into the chest), diverticulitis and diverticulosis (weakening and infection of the colon wall), hemorrhoids, anal fissures and fistulae.
Most sickness and health problems ASSOCIATED WITH SEVERE CONSTIPATION start from a toxic colon. Toxic megacolon is a life-threatening complication of other intestinal conditions, characterized by a very dilated colon, abdominal distention, and sometimes fever, abdominal pain, or shock. Colon cleansing usually eliminates the underlying causes of stomach pain.
The record at A-6 documents a respiratory rate of 18, on admission. The normal adult respiration rate is 12 to 18 breaths per minute. however, the respiratory rate is a sensitive and nonspecific indicator of respiratory dysfunction - changes may suggest Opioid -induced fluctuations in breathing or irregularities.
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 inside of the upper chest between and in front of the lungs ( the mediastinum), that had also been done on the same date were found to be "NEGATIVE". The purpose of the mediastinoscopy is to show whether cancer or tumors have spread to the mediastinal nodes. Problems with damage to internal organs, infection, and bleeding are possible and can also be detected from the mediastinoscopy. From that record it seems clear that NO clinically detectable metastasis were found.
The mediastinum is the space behind the sternum (breastbone) in the middle of the chest that separates the lungs. It contains lymph nodes, the heart and its great vessels, the trachea, the esophagus, and the thymus gland.
What the family had found to be peculiar however, was a dramatic voice change following the mediastinal procedures, what I assume to be an iatrogenic (doctor caused) type of voice disorder , a hallmark feature of a "partial vocal fold paralysis". However, Arlene Berry had began to regain her voice on the days prior to her death.
Vocal cord paralysis and voice change may follow laryngeal injury. due to Iatrogenic injuries of the membranous trachea.
A-20 of the hospital record documents a Creatine Kinase (CK) level of only 40 units per liter (U/L). In females, total Creatine Kinase should be 10-79 units per liter (U/L). 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. Creatine kinase (CK or CPK) is an enzyme or type of protein found in muscle and brain that leaks out and is released into the bloodstream when muscle is damaged. In normal conditions, there is very little creatine kinase circulating in the blood of the average, healthy human being. CK helps cells make the energy needed to move: may also be tested from the record.
The CK level usually parallels a disease activity.
Muscle wasting is a hallmark of a number of diseases, including cancer, bacterial sepsis, AIDS, diabetes, and end-stage heart, kidney, and obstructive pulmonary disease. Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients. Skeletal muscle atrophy is a common comorbidity of cancer. The progressive depletion of skeletal muscle is a hallmark of many types of advanced cancer. However, a clinical feature of demyelination is muscle weakness without muscle atrophy. Persons with Muscular Dystrophy and other neuromuscular disorders have low creatine kinase levels. Hypokalaemic periodic paralysis has a predilection for thyrotoxicity in some patients. It is associated with a low potassium concentration and a normal creatine kinase level. Guillain-Barré syndrome is characterized by ascending muscle weakness. Lyme disease may also cause weakness secondary to peripheral neuropathy but it does not produce evidence of muscle inflammation such as elevation of the CK. West Nile virus encephalitis may present with muscle weakness and flaccid paralysis. West Nile virus may cause a neurologic syndrome mimicking GBS. FIRSTConsult Normal creatine kinase levels do not rule out significant neuromuscular disease.
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. In patients with severe, longstanding heart failure, cardiac cachexia may mimic the cachexia that occurs in patients with disseminated malignant disease.
Essentials of the Diagnosis of Heart Failure
Studies of cachexia in parasitic infection
Persons with cancer have high CK levels.
Elevation of CK may be seen in stroke, extreme shock, or brain tumor(s). A very high creatine kinase value indicates severe muscle fiber breakdown (necrosis). Even in paraneoplastic disorders the serum CK level is typically elevated 8-100 times normal. Persistent or ongoing muscle injury will maintain high CK concentrations. The hallmark of muscle damage is elevation of creatine kinase ( CK ) concentration, which is also present in all patients with rhabdomyolysis. During episodes of acute muscle breakdown (rhabdomyolysis), CK levels can temporarily go off the scale, topping out at 50,000 to 200,000 U/L. Other forms of muscle damage, such as from a fall, a car accident, surgery, or a shot, can also increase CK. CK levels usually rise significantly in about 2 to 3 hours or perhaps a little longer (can rise two-fold within six hours) and peak within 24 hours.
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.
Low-grade inflammation may play a role in the etiology of the metabolic syndrome. a combination of medical disorders that increase one's risk for cardiovascular disease and diabetes. Toxic and metabolic myopathies probably are underrecognized in patients receiving treatment for cancer. With iatrogenic injury, laboratory investigations are of limited value in diagnosing this condition because the patient might not live long enough to make the connection, primarily due to iatrogenic neglect.
The Outpatient Record at OP-53 documents "pale-looking and lethargic". Paleness may be the result of decreased blood supply to the skin/cold, fainting, shock, or decreased number of RBC's (red blood cells), a hallmark of anemia.
Lethargy may be caused by the toxic effects of waste products on brain function. Lethargy and drowsiness are also associated with moderate to severe dehydration, including congestive heart failure. The same record 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, aspirin, NSAIDs (non-steroidal anti-inflammatory drugs). Compare Salicylate Toxicity with dangers of acetaminophen .
Caveat: An overdose of analgesics containing acetaminophen may cause damage within hours.
From the record it is clear that Arlene Berry had a history of "opiate" pain reliever use, including Aspirin (ASA), Acetaminophen (Tylenol), and a whole array of other medications, the combined effects of which are highly questionable, as evidenced by her Rx List, which undoubtedly can result in increased somnolence, alterations in speech patterns or dysarthria, and haemodynamic changes. Common drug side effects, include nausea, vomiting, sedation, dizziness, headache, weakness and stomach pain.
Dizziness, drowsiness, lethargy, and ataxia have all been cited with adverse events, including slurred speech, syncope, GI: constipation, nausea, vomiting, incontinence, and urinary retention.
Indeed these are the very same signs and symptoms that Arlene Berry had devoleded prior to her admission to the Kirkland and District Hosptal on May 23rd of 2000.
What I take to be the Health Management Record from the Kirkland and District Hospital at
A-21 of the record documents her sensory cognitive perceptual pattern as "sedated", a sign of acute or late toxicity, such as seen with adversities to various medications. Such patients often have a rather toxic appearance. Oversedation can lead to adverse outcomes. Compare findings associated with Toxic Myopathies in the setting of drug-induced iatrogenic myopathies with TOXIC NEUROPATHIES. See also Guillain-Barre Syndrome (GBS).
The so-called Miller Fisher syndrome is a variant of the GBS, characterized by disproportionate involvement of cranial nerves and the presence of cerebellar signs. Miller Fisher syndrome is a rare, acute polyneuropathy characterized by ataxia (abnormal muscle coordination), ophthalmoplegia (paralysis of the eye muscles), and areflexia (absence of the reflexes). The disorder is a variant of Guillain-Barre syndrome. (Source: excerpt from NINDS Miller Fisher Syndrome Information Page: NINDS) . Miller Fisher Syndrome
Miller-Fisher syndrome mimicking intracranial hypertension
eMedicine - Guillain-Barré Syndrome : Article by Andrew Miller, MD
What I take to be a continuation of the same record at A-21 and A-23 documents a "slurred" speech as evidenced by a  in the upper left corner, a distinct sign of condition such as Drug intoxication, in which dysarthria is a prominant finding in the setting of iatrogenic drug-induced myopathies. Myopathies can result from endocrine disorders, infection or inflammation, drugs, and mutations in genes. An acutely ill, toxic appearance is also a common feature in serious infections.
Endocrine Emergencies Slide
AES Abstract
eMedicine - Metabolic Disease & Stroke: Hyperglycemia
Skeletal muscle weakness is the hallmark of most myopathies such as seen in Guillain-Barre syndrome (GBS), a demyelinating disease that is most often seen several weeks after a variety of nonspecific viral, or other infectious diseases.
Guillain-Barre Syndrome typically follows a respiratory or gastrointestinal illness, immunization, trauma, or metabolic insult. and has been particularly associated with West Nile Virus Encephalitis. Viruses cause most forms of encephalitis. Several variants of GBS are recognized. These disorders share similar patterns of evolution, recovery, symptom overlap, and probable immune-mediated pathogenesis. Thus, GBS is seen to be a postinfectious immune-mediated disease. GBS frequently follows a flu-like illness. Several disorders, such as acquired hypokalemia, myasthenia gravis, periodic paralysis, and polymyositis, have symptoms similar to those found in GBS.
NEUROMUSCULAR DISORDERS:
In the last day or two of her life Arlene Berry tended "pulling to the right" when walking, a sign of ataxia (lack of motor coordination), or vascular limb ischemia (restriction of blood flow due to arterial stenosis or occlusion: it presents as a chronic inflammatory process), or toxic condition.
The lower limb is often ischemic in diabetes. Fecal impaction as a cause of acute lower limb ischemia. is reported in PubMed.
From the record it seems clear that there was every indication that Arlene Berry was about to suffer a catastrophic decline, at least from foreseeable dehydration due to decreased oral/water intake and excessive vomiting over the previous week, or more, which ought to have prompted immediate medical attention but did NOT. Water is necessary for the distribution of nutrients to cells, elimination of waste, regulation of body temperature, and countless other complex processes. On average, one can live only four days without water.
Dehydration is a condition in which water or fluid loss (output) far exceeds fluid intake. The body becomes less able to maintain adequate blood pressure, deliver sufficient oxygen and nutrients to the cells, and rid itself of wastes.
The emergency 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" and a prescription for Ciprofloxacin (Cipro), for treatment of Urinary Tract Infection. Cipro is an antibiotic indicated in the treatment of a variety of infections, including the flu. The healthcare provider who saw her made a diagnosis of "UTI". The belated test result however, what I assume to have been a urology test, or a blood culture test, evidenced at OP-55 of the Outpatient Record, later returned a finding of " NO Growth". According to my research, a negative urine test can suggest the presence of unusual bacteria or viruses causing symptoms of UTI. According to the record she was "Here 1 week ago for UTI. Last period on 6th of May".
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 had then been directed to the attention of the patient's "family MD", namely, Dr. Jordan.
CAVEAT: Prolonged use of ciprofloxacin may result in the overgrowth of nonsusceptible organisms. Cipro can potentiate existing renal insufficiency and has been implicated in several cases of acute renal failure. Careful observation of the patient is essential, and if superinfection should occur during therapy, appropriate measures should be taken.
American Kidney Fund Cautions Against Unwarranted Use of Cipro
N-9 of the nurses' notes documents a precaution for a "resistant bacteria", as evidenced by a 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. Further, details with respect to the offending organism were omitted from the record, withholding that information from the patient's family.
Onset of menstrual period as evidenced at OP-53 is closely related (within time frame) to illness in which symptoms result from production of toxin, possibly staphylococcus, which may then wash backwards up through the vagina, uterus and fallopian tubes, or similar mechanism to be absorbed from the peritoneal lining inside the abdomen.
Case reports cited primarily in women having period in which a blood-soaked tampon may provide an excellent breeding ground for the bacteria which causes Toxic Shock Syndrome (TSS), and is a significant cause of urinary tract infections. TSS may present just with circulatory collapse, with or without a rash and with or without fever. Staphylococcus aureus, a bacterium that can release toxins into the bloodstream, is believed to cause this illness. Methicillin-resistant Staphylococcus Aureus (MRSA) Infections. requires implementation of strict infection control policy which in this case had NOT been done.
According to her Rx List , Arlene Berry had also 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".
Additionally she had been given Statex (a narcotic: opioid agonist analgesic used to relieve pain) which also belongs to a class of the morphine family.
Submit that abdominal or stomach pain concurrent with nausea and vomiting points to the "abdomen" as the source of the problem . Abdominal pain can also be the result of "intestinal ischemia". The hallmark of intestinal ischemia is "abdominal pain".
Intestinal ischemia occurs when blood supply to digestive system is reduced. Intestinal ischemia due to mesentaric venous thrombosis is caused by a blood clot blocking a vein in the intestines which compromises the blood supply to the intestines giving rise to serious infection which can result in gangrene and tissue death leading to sepsis, or septic shock.
The presentation of abdominal abscess is similar to that of peritonitis, but the symptoms are generally milder.
The record at OP-54 dated May 22nd of 2000 documents a "haggard appearance" including "large blood trace leukocytes". Notably also, leukocytes (WBC's) are elevated with dehydration, hyperviscosity secondary to dehydration, and infection. Leukocytosis is the presence of an elevated WBC count.
Ameba only multiplies rapidly if a person is very run down by a deficiency, illness or infection.
The most common signs of amebic infection are alternating diarrhea and constipation (possibly accompanied by blood and excessive mucus) and irregular appetite. Other clinical signs include vomiting, listlessness,weakness, low weight and signs of dehydration (e.g.sunken eyes, thick oral mucus). If the lungs are infected (a condition generally associated with more chronic infections), labored breathing, mouth/nasal discharge and wheezing may be noted.
A-19 of the record documents a WBC (white blood cell) Count of 22.4 H. White 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 Compare : Lab Values
Polymorphonuclear leukocytes predominate in bacterial infections, whereas lymphocytes predominate in tuberculous and nonbacterial infections. In fact, leukocytosis often reflects a favorable prognosis by signaling that the patient's bone marrow is producing WBC's in response to an infectious or inflamatory process. View
The record at A-19 documents a Lymphocyte Count of 2.0 L (low) suggestive of lymphocytopenia in which lymphocytes are reduced with nutritional deficiency, infection or an exhausted immune system. Lymphocytopenia causes may arise from accelerated destruction of T cells or other syndromes associated with depletion of blood lymphocytes. Interestingly, iatrogenic lymphocytopenia is caused by radiation therapy, marked by a reduction in the absolute number of T cells (lymphocytes are the most sensitive to whole body radiation and their count is the first to fall in radiation sickness. The same record documents an Absolute Lymph’s (Lymphocyte) Count of 0.4L (low), suggestive of ascites due to fluid build-up in the abdomen in which liver disease, or heart failure are the most common causes. If the ascites is due to liver disease the fluid may be clear to “yellowish”, uninfected and have a low T cell count. If bacterial infection is present in ascites this may suggest spontaneous bacterial peritonitis in which abdominal pain is a prominent finding. (If peritonitis is not treated promptly and effectively multisystem organ failure occurs rapidly).
Chronic anxiety, panic, stress and depression have been shown to compromise health, damage immune function, and result in symptoms identical to AIDS. Any doctor can make a clinical diagnosis of "adrenal insufficiency". But the symptoms of that condition can ALSO mimic AIDS symptoms. Meanwhile, medical stupidity continues to dispense toxic medications that mimic AIDS, while life-saving clues are either ignored or censored.
The four clinical AIDS symptoms are identical to those associated with conditions that run rampant on the African continent such as malaria, tuberculosis, parasitic infections, the effects of malnutrition, and dysentery.
Mental stress provokes production of the hormone cortisol; excessive cortisol causes rapid and dramatic reductions in T cells, a condition known as lymphocytopenia. Within minutes, stress induces cortisol levels to increase as much as 20-fold. High levels of cortisol can eventually cause what medical texts describe as "significant atrophy of all the lymphoid tissue throughout the body" which may lead to "fulminating infection and death from diseases that would otherwise not be lethal."
The hallmark of acute bacterial infection is the presence of polymorphonuclear leukocytes. Leukocytosis (especially neutrophilia) indicates systemic infection. Leukocytosis is rare in the absence of bacterial superinfection. There is a positive correlation between the number of bacteria and the number of polymorphonuclear leucocytes.
Leukocytes have the potential to lyse E. histolytica trophozoites and vice versa. E. histolytica is cytolytic to human leukocytes on contact. Only virulent amoeba canlyse polymorphonuclear leukocytes (PMNs).
Pathogenesis of infection by Entamoeba histolytica
The ANC or Absolute Neutrophil Count, in this case, is within in the normal range, with a count of 5152. ANC (absolute neutrophil count; basic measure of immune system). ANC is the real or actual number of white blood cells that a patient has to fight an infection. White blood cells are the part of the patients blood that work against possible bacteria, fungus, or viruses that may make the patient sick. A normal ANC is 2500-7000.
Generally, an ANC above 1,000 means that the patient's infection fighting ability is in the normal range.
Neutrophilia (or neutrophil leukocytosis) is a condition where a person has a high number of neutrophil granulocytes in their blood. The neutrophil count in blood is a good indicator of a person's ability to fight bacterial infections. Neutrophilia occurs when bacterial infection sends signals to rapidly increase the output of neutrophils from bone marrow. If the infection is severe enough, bone marrow output of neutrophils becomes greater than neutrophil migration into the infected tissue, which increases blood neutrophil counts. This is a normal healthy response to infection. Neutrophils, are also known as "segs", "PMNs" or "polys" (polymorphonuclears). They are the body's primary defense against bacterial infection and physiologic stress. Neutrophilia most often occurs secondary to inflammation, stress or certain medications. An increase in white blood cells and neutrophilia occurs 4 to 8 hours after elevation of stress hormones and return to normal 1 to 3 days after.
Wegener's Granulomatosis is a rare disease of uncertain cause. Wegener's granulomatosis is a form of vasculitis that may affect many parts of the body, including the brain, nerves, eyes, sinuses, lungs, kidneys, intestinal tract, skin, joints, heart, and other sites.
What is Wegener's granulomatosis? Compare Granulomatous amoebic encephalitis.
Wegener's granulomatosis, granulomatous cerebral amebiasis, vasculitis, and heart attack are high on the order of Neutrophilia in combination with this patient's associated signs and symptoms. Ameba can spread hematogeneously from a cutaneous, ocular, or pulmonary lesion to the CNS, where vasculitis may also dominate the clinical picture.
An ameboma may simulate an adenocarcinoma or another granulomatous process. Ameboma, the forgotten granuloma?
"Granuloma" formation is a hallmark of chronic bacterial infection. Granulomas are localized, protective inflammatory reactions initiated by CD4[+] T cells (lymphocytes), which contribute to control of bacterial growth and blockade of bacterial dissemination."
http://cat.inist.fr/?aModele=afficheN&cpsidt=14161000
Amebic granuloma--an experimental study.
Lymphopenia (also called lymphocytopenia) can occur concurrently. If the total white blood cell count is high due to a rise in neutrophils and eosinophils, then an allergic or parasitic process is most likely.
Rises in lymphocytes can indicate cancer. In this case we have a significant reduction.
A right shift is present only when the mature neutrophil count is above the normal range. A “shift to the right” implies an increase in hypersegmented neutrophils. Less mature neutrophils - those that have recently been released from the bone marrow into the bloodstream - are known as "bands" or "stabs". Stab is a German term for rod. A right shift generally indicates chronic infection/chronic inflammation. A right shift is present when the band (immature) neutrophil count within or perhaps lower than the normal range, which in this case is normal at 3.0 (normal <6.0).
When there are more neutrophils than expected there is said to be a "left shift," also indicative of disease processes such as infection. .If a patient was very dehydrated the blood would be more concentrated and may appear to have more WBC's. This shift is caused by a stimulus of the cell factories in the bone marrow. Bone marrow infiltration by leukemia, myeloma, lymphoma, or metastatic solid tumors (eg, breast, prostate) can impair neutrophil production. That is NOT the case here.
Emigration of neutrophils, together with tissue destruction is the hallmark of abscess formation. These lesions are commonly produced by a group of microorganisms known as the pyogenic (pus-producing) bacteria). The staphylococci are a group of bacteria possessing pyogenic properties.
A marked polymorphonuclear leucocytosis, positive blood culture, elevated serum enzymes and alkaline phosphatase are characteristic of this condition. It may not be possible to differentiate between amoebic and pyogenic abscess on clinical grounds, routine investigations and imaging techniques. Activation and accumulation of PMNs is one of the initial events of tissue injury, which triggers the release of oxygen free radicals, arachidonic acid metabolites and lysosomal proteases, with subsequent tissue injury (Fantone & Ward, 1982).
The interaction of human polymorphonuclear neutrophils (PMNs) with two strains of Entamoeba histolytica that exhibit different degrees of "virulence" is reported in Medline. Cerebral amebiasis is a rare cause of brain abscess and is characterized by an abrupt onset of mental status change and/or focal neurologic deficits. Progression to death occurs over 12-72 hours without adequate treatment. eMedicine - Amebiasis : Article by Robert Swords, MD
The increased sensitivity of infections in diabetes has long been associated with changes in PMN functions. Studies suggest that insulin treatment may normalize PMN functions. Although infections appear to be more common and more severe in diabetics, there is no evidence that diabetics are at greater risk for all infections in terms of frequency and mortality.
In vivo evidences that insulin regulates human polymorphonuclear neutrophil functions is reported in the literature.
A-19 documents a Red Blood Cell (RBC) Count of 4.30 (3.80 - 5.80 is normal) with a Hematocrit (HCT) Count of 0.361 L (low), suggestive of anemia.
Flag: Counts that are above or below the reference range are recorded in the flag column, and marked with an ‘L’ for low or ‘H’ for high.
HCT is the measurement of the percentage of red blood cells (RBC) in whole blood with a reduction suggestive of anemia. Most common reasons for a falling HCT include loss of blood (traumatic injury, surgery, bleeding colon, nutrition deficiency, kidney failure). Other reasons for a low HCT include dehydration, iatrogenic fluid overload, or vasoconstriction following acute blood loss. The hematocrit (HCT) is another way of measuring the amount of HEMOGLOBIN (Hb), and in this case it is very low. Also a hallmark of exertional fatigue, as seen in patients with chronic heart failure and is usually attributed to skeletal muscle underperfusion. A lowered red blood-cell count, however, may cause dizziness and fatigue with blood pressure insufficient to supply oxygen and glucose to brain. Anemia is present when HCT is < 37% in women.
A low HCT is also associated with compromise of oxygen delivery.
MiscInvestigations
If your blood cells are really small, then the hematocrit can be low even if you have the appropriate number of red blood cells.
Possible causes of the symptom Anemia
Caveat: Signs of blood loss, such as shock, hypotension, and a falling hematocrit level are all associated with "trauma". The most common cause of a falling hematocrit is loss of blood. It can take 24 to 72 hours post trauma to reflect the true volume loss.
A-19 documents an RDW (red blood cell/raw distribution width) of 18.4 H (high): RDW's principal function is to transport oxygen to the blood and becomes elevated with oxygen deprication and is also increased with anemic hemoglobinopathy (loss, an iron deficiency anemia and an allergic white blood cell picture), a hallmark of of Anemia. When there are insufficient RBC's (red blood cells), oxygen delivery is compromised). Normal RDW for an adult female are 12-16 g/dL, and 14-18 for an adult male.
A-19 documents a Hemoglobin with a Count of 120, (reference 120-160). Hemoglobin carries oxygen supply to vital organs.
Normal Values: Female: 12.1 to 15.1 gm/dl.
Facts suggest inadequate oxygenation despite the fact that oxygen levels were returned to normal by compensatory mechanisms, marked by a clinically evident inability to adequately ventilate or oxygenate the patient. Hemoglobin (Hb), the main component of red blood cells, is a protein that carries oxygen from the lungs to the body's tissues, and carbon dioxide from the tissues to the lungs to be exhaled.
CAVEAT: dehydration can temporarily increase hemoglobin levels giving rise to false test. Warning signs for abnormally low hemoglobin levels are fatigue, fainting, pallor (loss of normal skin color), and shortness of breath.
A-19 documents an Absolute Mono's of 0.60 (normal 1.0 - 4.5). The Absolute monocyte count is age dependent; Count rarely exceeds >1.0 x 109/L The monocytes are a type of phagocyte which mature into macrophages, important germ eating cells. Search key term for "phagocytes". Patients with a low monocyte count have a higher risk of getting sick from an infection, particularly those caused by bacteria.
In cancer, leukemia, or with neoplasms (malignant effusions), the monocytes become elevated. In this case the monocyte count is well below the normal range.
A-20 documents an O2SATURATION - arterial oxygen saturation (SaO2) of 98.9 H with an evident run time of 1720 hours on May 24th of 2000, notably, several hours following the patient's alleged time of death. Oxygen to achieve O2 saturation is >90%, however, a relatively high O2 saturation can also be a sign of obstructed breaths. Also, one's oxygen saturation should NEVER drop below 96 %. N-3 of the record documents an "O2Sat dropping" at 0320 hours, while the record at A-26 documents an SaO2 of 80 as early as 0220 hours followed by a rapid drop in Blood Pressure to "78/70" at 0235 hours, only 5 minutes later.
Low arterial oxygen pressure strongly aggravates brain damage. In fact, the level of oxygen saturation can cause dyspnea (shortness of breath) by inducing panic and fear. Further, elevations in carbon dioxide levels appear to stimulate dyspnea. Panic, in turn, can stimulate increased ventilatory effort, which can result in more fatigue and increased panic - a vicious cycle. Panic, fear, and anxiety are common affective components of dyspnea. Cognitive processes commonly trigger affective responses. In this case leading to exertional fatigue due to skeletal muscle dysfunction (underperfusion) in patient. Exertional fatigue, sleep loss, and negative energy balance may result in Heart failure . Profound fatigue is associated with panic disorder. Moreover, post-exertional fatigue and flu-like symptoms were predictive of lowered cardiac output, a hallmark of CFS. These factors could create deficiencies in blood flow to organs and muscles. Further, people who are predisposed to panic and anxiety attacks are also more prone to sleep paralysis.
CO2 build-up and oxygen deprivation are the critical factors that result in dyspnea.
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 , which is also evidence of "impaired organ perfusion" (infected material can block blood vessels to the heart and brain resulting in an inferior ischemia, or an ischemic cascade, a series of biochemical reactions that take place in the brain and other aerobic tissues after seconds to minutes of ischemia. Loss of blood flow to the brain results in neuronal injury due to both the cessation of blood flow leading to oxygen and nutrient deprivation and the initiation of secondary mechanisms (Dawson & Dawson, 1997). This neurotoxic cascade involves derangement in normal metabolic and physiological functions as well as recruitment of cell death processes.
Reduction in blood flow (relative ischemia) impairs oxygen delivery and causes cerebral hypoxia. The hallmark of reperfusion injury after brain ischemia is an "inflamatory reaction" which can result in shock and circulatory collapse, marked by a rapid drop in the blood pressure.
The Outpatient Record record also documents "bloody bowel movements for 4 days", a sign of possible diverticulitis, a condition associated with constipation , marked by abnormal increase in the white blood cell (WBC) Count, indicative of infection, and blood in the stool (concealed hemorrhage) or passage of bloody stool. (See also: Abdominal Pain )
Stomach pain concurrent with nausea and vomiting points to the "abdomen" as the source of the problem.
The features of abdominal migraine is an abrupt on-set of severe abdominal pain followed by an abrupt discontinuation of symptoms. Abdominal migraine is one of the variants of migraine headache, ie. ( headache lethargic migraine) . A strong family history of migraine headaches is a common finding. Recurrent vomiting is a hallmark feature of CVS ( cyclic vomiting syndrome) View: Nausea and Vomiting: Principles of Therapy
The most common triggering agents for migraines are alterations in serotonin metabolism (a deficiency), diabetic condition, hormonal imbalances, histamine-induced platelet aggregation (blood platelets sticking together) blood sugar imbalances and certain medications. In women, migraine attacks may also be triggered by hormonal changes, for example during menstruation (periods).
Migraine variants
Intestinal malrotation may be difficult to diagnose.. The symptoms may be vague in nature, because of the association of vomiting and pain; initial episodes of partial obstruction may be mistaken for bouts of flu-like illnesses. The hallmark of this problem is the presence of bilious vomiting associated with abdominal pain and constipation. Vomiting can be very severe and feculent and or bilious after several days of no BM. Notably, constipation, fecal impaction and bowel obstruction are common problems for oncology patients. Conditions listing complications include constipation.
Cyclic Vomiting Syndrome (CVS) may overlap with other digestive disorders like delayed gastric emptying, or gastroparesis. CVS is sometimes mistaken for gastroparesis, a complication of diabetes.
Hyperglycemia marked by high blood glucose has been shown to induce a state of functional gastroparesis. Not only does hyperglycemia contribute to developing gastroparesis; short-term hyperglycemia exacerbates gastroparesis: is a prominant finding in Diabetic Neuropathy . Elevated serum glucose levels and reduced albumin are risk factors for nerve dysfunction, as is prolonged intensive care unit stay.
Polyneuropathy may develop after only one week of the systemic inflammatory response syndrome. The clinical entity critical illness polyneuropathy occurs almost exclusively in patients in critical care units and has been characterised as a complication of sepsis and multiple organ failure. It is associated with profound muscle weakness. in association with iatrogenic neglect and the failure to undertake regular bedside neurological and electrophysiological examinations in critically ill patients. Severe axonal motor neuropathy after acute respiratory failure probably represents a variant of "critical illness polyneuropathy" that can be recognized from the temporal course of a conversion from primarily pulmonary to a pattern of neuromuscular ventilatory failure, and may be preceded by weakness with only minimal movement or complete paralysis in response to speech. Accordingly, the differential diagnosis of CIP is equally lengthy, consisting of drug-induced weakness, myasthenia gravis, myopathy, atrophy, Guillain-Barré syndrome, polyneuropathies caused by infection.
Critical illness polyneuropathy is an ICU-acquired neurologic crises that affects the peripheral nerves, muscles, and neuromuscular junction. Most ICU neuropathy patients who survive their underlying illness will recover nerve function. Clinical recovery may take weeks in mild cases and months in severe cases. The majority of survivors may have persistent functional disabilities and a reduced quality of life.
CAVEAT: DRUG INDUCED MYOPATHY - The onset of clinical manifestations of drug-induced myopathy usually develops insidiously and can occur from days to months after exposure to the causative agent. Commonly, patients present with nonspecific complaints of progressive, generalized muscle weakness (diffuse weakness) muscle pain (myalgia), or fatigue. Proximal or diffuse muscle weakness of the arms and legs is the hallmark symptom in Toxic Myopathies and infections in hypokalemic myopathies. Compare Muscle wasting and diffuse weakness in combined effects of sepsis and multiple organ failure, and such as seen in encephalitis and meningitis.
Neuromuscular sequelae of critical illness.
Critical illness poly-neuropathy, an important cause of failure to wean from assisted ventilation is often missed due to iatrogenic neglect.
Bowel ischemia (a lack of proper blood flow to the intestines may result in bloody or tarry stools.
A-20 of the Laboratory Discharge Summary documents a Serum Potassium level of 3.4 L (low) suggestive of Hypokalemia (not enough potassium in the blood) which leads to an electrolyte imbalance which can rapidly progress to weakness, fatigue and cardiac problems. When serum potassium is less than 3.5, the condition hypokalemia is suggested. The condition is also known as potassium deficiency and is associated with excess water loss, such as from dehydration (the first sign of hyperosmolar dehydration with hyperglycemia may be syncope). Anything below 3.5 creates a serious risk of cardiac arrhythmias leading to cardiac arrest. In addition, loss of potassium and volume contraction from vomiting may also potentiate metabolic alkalosis. Hypokalemia can result from a variety of medical conditions or medications which require close monitoring as there is a risk for IV volume overload such as hyponatremia, and worsening hypokalemia, usually due to lack of established diagnostic criteria.
Hypokalemia may contribute to development of demyelination.
Hypokalemic periodic paralysis is a congenital disorder characterized by episodes of flaccid muscle weakness (low potassium levels may cause the symptoms of headache, muscle weakness, muscle cramps, and fatigue) that causes intermittent episodes of paralysis. The attacks can occur from daily to yearly and may last for a few hours or for several days. Potassium is essential for many body functions, particularly muscle and nerve activity.
Hypokalaemia is commonly caused by medication.
In this case, No serum potassium replacement was ordered, or administered, in this case. It is not known what the patient's potassium level was at the time of her admission. No lab tests were performed soon enough to verify, or treat accordingly. The most common problems associated with reduced potassium levels are hypertension, congestive heart failure, cardiac arrhythmias, depression, and fatigue. A variety of conditions can cause the loss of potassium from the body. The most common of these conditions are vomiting, diarrhea, and other gastrointestinal problems.
Reference.com/Encyclopedia/Hypokalemia
Some of the symptoms of Hypokalemia incude:
See full list of 8 symptoms of Hypokalemia
See full list of 633 symptom search combinations related to Hypokalemia
Metabolic disturbances (such as decreased potassium levels) may result in paralytic ileus, marked by abdominal distention, and absent bowel sounds.
Medication Induced Causes of Constipation
Untreated constipation and/or fecal impaction can lead to bacterial overgrowth, especially in patients with high levels of glucose in the blood.
Digestive problems are relatively common among people with diabetes. The most common is constipation, affecting nearly 60% of people with diabetes.
The record at OP-53 documents "Here 1 week ago for UTI. Last period on 6th of May" . UTI with or without fever can be a a sign of potential severe kidney infection. The most serious UTI is infection of the kidney (pyelonephritis). Most UTIs are caused by bacteria. Usually by the bacteria that are found in the intestines. Amebiasis, normally an infection of the intestinal tract, may spread and infect other organs such as the liver or brain. Infection of the brain can be fatal. Amebomas may produce symptoms that mimic cancer or other intestinal diseases.
Gastroparesis affects up to 75% of people with diabetes.
Autonomic neuropathy is a group of symptoms caused by damage to nerves supplying the internal body structures that regulate functions such as blood pressure, heart rate, bowel and bladder emptying, and digestion.
Gastroparesis shows a strong female predominance, and menstrual cycles are important; in the week before menses, when progesterone levels are high, nausea and vomiting can be exacerbated. Patients with Gastroparesis have emesis of undigested food consumed many hours or even days previously. Gastroparesis may occur in relation to systemic diseases such as diabetes mellitus. Diabetics with autonomic neuropathy may also delelop Neurogenic Bladder. For some females -- a clear pattern may be seen following the menstrual period, especially in patients with a suspected UTI.
Severe constipation may also be the result of dehydration (water insufficient to rid body of wastes); can result in perforation and fecal compaction. Patients with severe constipation also are more prone to UTI's. |
Bloody stools may signify bleeding stomach, diverticular bleeding intestinal infection (such as bacterial enterocolitis), c lostridium difficile colitis , or volvulus . C. difficile is recognized as the major causative agent of colitis (inflammation of the colon). C difficile colitis can develop during or up to 8 weeks after taking antibiotics - is an increasingly aggressive iatrogenic disease. Other forms of colitis to consider include amebic colitis, ulcerative colitis, and granulomatous colitis which often lead to toxic dilatation of the colon, which often mimic other enteric infections. The appearance of amebic colitis may resemble that of inflammatory bowel disease.
Antibiotics may not cause side effects until they have built up in the body for several days - (See WARNINGS)
Constipation is also an occasional symptom of C. difficile colitis in the setting of ileus. Other possible problems having similar signs and symptoms to consider are Intussusception (medical disorder), and bowel obstruction, for example.
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.
According to the record at A-6 she returned to the ED (Emergency Department) on May 23rd of 2000 with "the very same complaints". 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, "she was given antibiotics and sent home" , as evidenced at A-8 of the hospital record.
Rapid evolution of illness and patient return within 24-48 hours suggests a severe illness.
Arlene Berry was also rejected for moderate dehydration due to excessive vomiting on the days before, which had been grounds for admission at that time; suggests incompetence, negligence, and substandard care. Public funds are for patients, not profits, and certainly NOT for superficial renovations to bolster corporate ego's.
On examination the physician who saw her documented positive "bowel sounds" that is consistent with physical findings of hyperactive bowel sounds , also a sign of gastropareses in clinical diabetes which can rapidly progress to intestinal obstruction. Hyperactive bowel sounds occur early as GI contents attempt to overcome the obstruction. An Intestinal obstruction is a partial or complete blockage that results in the failure of the intestinal contents to pass through the bowel. Absent bowel sounds after a period of hyperactive bowel sounds are significant findings which can indicate that rupture of the intestines, or strangulation of the bowel with subsequent bowel tissue death ( necrosis ) may have occurred.
MEDArticleMgr
Clinically, bowel obstruction presents with an abrupt onset of low abdominal pain, low-grade fever, nausea and vomiting sometimes mimicking symptoms of acute appendicitis.
OP-53 documents a history of "bloody bowel movements when voiding" for "4 days" and also that she was pale looking and lethargic . Pale skin suggests decreased blood supply to the skin.
The record at A-6, what I take to be Dr. Spiller's physical examination, documents a "soft, non-tender" abdomen, with "no rebound tenderness", and "no masses". Rebound abdominal tenderness is common but nonspecific in liver trauma, but masses, on the other hand, can suggest either a growth, or lession(s). The record clearly documents "no masses". There are NO records to suggest that the ED physician (Dr. Spiller) had ever bothered to take the time to perform a Complete Physical or NeurologicalExamination of this Oncology patient.
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. What appears to be a referral at A-6 of the medical record, a chart-copy from the admitting physician directed to the attention of the attending physician documents what I take to be an assumptive or provisional diagnosis of "vomiting", while the record at N-11 documents "vomiting, lung CA". Further, a question appears to have been raised (but also ignored) with respect to a suggested metastatic cancer of the brain, leaving the etiology of the vomiting and the stomach pain left undetermined for the attention of the patient's family MD, Dr. Jordan.
Jordan/Spiller = cross-covering physicians
Vomiting is NOT a diagnosis but rather 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 cholera means "bilious" - The word cholera is Latin for bilious disease, and has come to indicate a severe intestinal infection.
CAVEAT: the earliest amoebic lesions appear as small, yellow mucoid (yellowish exudate) elevations containing necrotic material where the parasite can be found.
Arlene Berry was still neurologically responsive when I saw here following her admission and in fact she was able to reach and use for herself the kidney basin at her bedside table as she occasioned to vomit more of the same "flu-like yellowish bile" (bilious, meaning "full of bile" ) 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 at N-6 documents that the patient had stated that she was then "feeling a little better", whereupon she was then assisted to bed. She complained of being "cold" (she had had the chills), a sign of venular constriction, and so the nurses provided her with extra blankets, as evidenced by that record. It also seems clear that she was at least benefiting from Intravenous Fluids (IV) at that time. Further, Arlene Berry had stated that she was "very tired" - infers diminished alertness or awareness.
A-26 documents a body temperature above 37.0 C (Fever has been defined as a body temperature elevated to at least 1 F above 98.6 F/37.0 C). According to the record the documented temperature is slightly < 38.0 C at approximately 37.8 C, indicative of a low grade fever.
CAVEAT: Temperature often does not respond to infection or toxic agents.
Initially,there was "emesis of yellowish fluid" documented at N-6, what is termed bilious vomit or frank bile, but a later episode documents a "large queery bloody emesis" seen at N-5 of the Nurses' Notes, suggestive of a more significant backup of intestinal material, ie. vomiting of fecal material (due to obstruction). Family was present to witness an episode of large chocolate coloured (gross appearance), odorless, pasty material, a hallmark of amebic infection. Amebic meningitis might be confused with toxoplasmosis, cytomegalovirus infection, and other opportunistic pathogens. CSF findings consistent with meningitis, and a CSF gram stain showing no organisms, ie. 'no growth'.
A history of frequent vomiting or bilious vomiting in the presence of abdominal pain should be a red flag suggesting the possibility of intestinal obstruction.
N-10 of the Nurses' Notes document the patient's level of care as "routine", which showed verySATlittle concern.
N-3 documents an "orally thick brownish secretions" at 0320 hours. Compare: Pleural Amebiasis: Isolated Organ Involvement
AMEBIC abscess contains brownish material and cellular debris (chocolate-brown abscess fluid is thought to be highly characteristic of amebic abscess).
The center of an amebic abscess, consisting of lysed hepatocytes, erythrocytes, bile and fat, may liquify and this necrotic material (sometimes incorrectely called pus) will range in color from yellowish to reddish brown.
At the time of her admission to the hospital, Arlene Berry's Blood Pressure was documented at 115/70, with a pulse of 79 and regular, a respiration rate of 18, with signs of "mild diffuse weakness", and "difficulty ambulating". Diffuse weakness may lead to respiratory insufficiency. A common cause of diffuse weakness is critical illness polyneuropathy and is associated with neuromuscular blocking agents, also suspicious for some type of systemic illness, as evidenced by the record at A-6. At the time of this assessment, Arlene Berry was found to be "alert and oriented", with "NO Focal deficits". Within a few hours of her admission she developed a rapid progression of muscle weakness and apnea.
MedlinePlus Herbs and Supplements: Phosphates, Phosphorus
eMedicine - Central Vertigo : Article by Keith Marill, MD
All about Guillain-Barré syndrome: GBS sub-families and variants.
Patient Resources
Infectious agents that are most commonly associated with muscle weakness including the flu, or flu-like illness. Weakness is a hallmark of the Guillain-Barre Syndrome (GBS), a disorder caused by nerve inflammation involving progressive muscle weakness or paralysis, which often follows an infectious illness. Since the widespread application of the vaccine preventing paralytic poliomyelitis, the number one cause of acute neuromuscular weakness in the developed world is Guillain-Barré Syndrome. The pathogenesis of GBS following an amebic or parasitic infection is not known, although Guillain-Barre Syndrome following malaria is reported: J infect 1999;38:48-50.  [PUBMED].
In this case however, osmotic demyelination, an iatrogenic disease related to inappropriately rapid correction of plasma osmolar disorders is suspected because acute paralysis in Guillain-Barré syndrome is related to a Na negligence. acute paralysis in Guillain-Barré syndrome is related to a Na negligence.
Rapid correction of chronic hyponatremia can cause osmotic brain demyelination . Positive association between blood brain barrier disruption and osmotically-induced demyelination by exposing substances normally excluded from the brain. Hyponatremia result from a deficit of sodium, or surplus of water. It occurs in patyients with meningitis, encephalitis, pneumonia,septicemia, severe malaria, bronchiolitis, RSV infection and Guillian Barre syndrome. Osmotic demyelination syndrome (central pontine myelinolysis). Central pontine myelinosis belong(s) to the category of Neurological conditions associated with Salt and Water Disorders, particularly Osmolality.
Central Pontine Myelinolysis consists of demyelination without inflammation in the base of the pons, with a relative sparing of the axons and the nerve cells.
Demyelination - Factbites
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, as evidenced at A-21 , seen (barely visible in the shaded box) in the upper left hand corner.
The record at A-20 documents a Glucose of 13.2 H mmol/L): >236 mg/dl. (the normal range is 4.1 - 7.8). High blood sugar usually comes on slowly. Elevated levels of blood glucose (hyperglycemia) lead to many problems. Hyperglycemia, or high blood glucose levels, is the hallmark of diabetes (usually occurs slowly, over several hours or days. It may be caused by: 1. not enough insulin 2. illness (such as a cold or flu) 3. infection 4. eating too much 5. stress 6. certain medications). Pre-diabetes is also a condition in which blood glucose levels are higher than normal. If your blood sugar levels remain high, and you become dehydrated, you are at risk of getting a life-threatening condition called hyperosmolar state or diabetic ketoacidosis. These are both medical emergencies. Caveat: Plasma glucose >120 mg/dl in the absence of diabetes = clinical sign of sepsis.
Hyperglycemia can lower the serum sodium concentration by 1.6 mEq/L for each 100 mg/dl. Hyperglycemia itself is a risk factor for "soft-tissue infections".
|
Hyperglycemia (an elevated blood glucose) is clearly associated with microvascular complications of nephropathy, retinopathy and neuropathy, and is also a contributory factor to the macrovascular complications of atherosclerotic vascular disease. Infection results in widespread microvascular leak,local thrombosis, and ultimately multisystem failure if un-treated.
Hyperglycemia is the metabolic hallmark of diabetes.
Changes in blood sugar levels can induce coma and other serious problems, including death. Signs and symptoms of diabetic ketoacidosis may also mimic those of the flu.
Symptoms of Untreated Diabetes |
The danger of this lies in the fact that if untreated , diabetes can damage the eyes (Read about " The Eye "), kidneys (Read about " Diabetes and Kidney Disease "), nerves, heart and blood vessels. (Read about " The Heart & Cardiovascular System "). Hyperglycemia Slows Mental Functions .
Diabetes is the leading cause of kidney failure, heart disease (heart attack, stroke), nerve disease, limb amputations, and blindness . Untreated, diabetes can lead to glaucoma, blindness and death.
Hyperglycemia appears acutely toxic in critically ill patients. Hyperglycemia (>110 mg/dl, >6.1 mmol/l) predisposes to ICU complications, prolonged intensive care dependency and death.
Hyperglycemia is the hallmark of diabetes and is associated with renal insufficiency and/or renal dysfunction. High blood sugar "Hyperglycemia", can rapidly progress to diabetic coma if not quickly recognised and/or left untreated.
Patients with diabetes may be more prone to infections of the bladder, skin, and vaginal areas, especially in the setting of hyperglycemia. The mechanism is thought to be inhibition of phagocytosis and leukocyte mobilization by hyperglycemia.
Patients taking antipsychotics should undergo fastingblood glucose testing first as they should also be monitored for symptoms of hyperglycemia (high glucose in the blood) including polyuria [urinating large volumes of urine]. No dangerous medications should ever be taken in the absence of a CBC and appropriate toxicology screening.
Women's Health Advisor 2005.4: High Blood Sugar (Hyperglycemia)
Microvascular changes in diabetes
Analysis of arterial and/or mixed venous blood provides information concerning the oxygenation, ventilatory, and acid-base status of the subject from whom the specimen was obtained
The evaluation of conduct of perfusion lays with blood gas analysis. Cerebral.html
A belated venous gas analysis revealed a
This patient clearly had vascular compromise of tissue in a part(s) of the body where there was lack of blood supply.
Most metabolic disorders that have neurological symptoms and signs can lead to coma if not adequately treated. Left untreated, a diabetic coma can lead to permanent brain damage - with a later development, progressing to unconsciousness and death. Patients with severe Guillain-Barré syndrome can appear to be "locked in."
Early symptoms of impending Diabetic Coma include polyuria , nausea, vomiting and abdominal pain, with lethargy and somnolence.
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 further evidenced at A-21 of the medical record. Further, there is absolutely nothing on record to suggest that any Supportive Care & Symptom Control Regimens were ever implemented.
From the record it is clear that NO diagnosis or differential diagnosis was made at that time, or at all, as evidenced by the record at A-3 . From the same record it is also clear that nothing was entered because nothing was done.
The record at A-12, what I take to be physician orders documents the concomitant administration of Senokot, MS Contin (morphine), also a narcotic analgesic, Statex and Gravol, an anticholingeric agent, including IV solution and additives, the most dangerous of which is the MS Contin. "Contin" is a pharmaceutical industry buzzword for "time-release" or "continuous" release. Some of their side effects are also caused by actions in the CNS.
MS Contin is a trade name for morphine sulphate. MS = Can mean morphine sulfate or magnesium sulfate. Often confused for one another. Magnesium Sulfate (also called epsom salts) is a mineral. It is also used as part of intravenous (IV) feedings (eg, TPN).
According to the record at N-6 she was admitted at 18:45 hours and had spent 75 minutes in the ER as evidenced at A-3 , placing the time of administration of morphine between 17:30 and 18:45 hours.
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 . A typical single dose of Stemetil for a small woman with low body weight is 5mg.
From that record it is clear that Arlene Berry had been ordered and administered a totally inappropriate and contraindicated medication while she was in an altered state of consciousness at that time, as evidenced on the record by extreme somnolence. Altered consciousness can result from decreased cerebral perfusion. This finding has been reported with depression, toxic brain exposure and in response to certain medications. Possible mechanisms of this relationship include increased ventilatory and sympathetic responses to hypoxia, decreased cerebral perfusion, and increased coagulability. The implication is that decreased cerebral perfusion pressure leads to decreased cerebral blood flow and oxygenation, which could damage brain cells.
Stemetil is not be administered in the presence of circulatory collapse, altered states of consciousness or comatose states, such as seen in patients with Pre-Diabetes (borderline or chemical diabetes), or diabetes mellitus.
Stemetil Can Kill You...!
The term "contraindicated" essentially means that the drug in question should not be given to a patient.
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 addressing any possible underlying causes. It seems clear that Dr. Jordan neglected to consider the etiology of the nausea and vomiting as a condition requiring prompt medical intervention. Instead, he elected to give her a brain damaging neuroleptic/antipsychotic drug without any review of her medical record. NO close monitoring or toxicological screening was done.
No simple blood tests were performed in a timely manner.
Arlene Berry developed focal neurological deficit after administration of the drug Stemetil, following co-administration of morphine which can adversely affect brain function by changing the chemical environment of the brain, afterwhich she began to deteriorate rapidly.
If you're going to deliver drugs by disrupting the blood-brain barrier, you're going to let in everything else in the bloodstream. Any breach in the BBB can lead to alterations in the CNS (central nervous system). Blood-brain barrier (BBB) disruption is accompanied by cerebral edema.
Once bacteria have established a foothold on the membranes surrounding the brain, they trigger inflammation severe enough to cut off the blood supply resulting in decreased cerebral perfusion and cause swelling in the brain. The decreased attenuation throughout the cereberal hemispheres may result in stroke symptoms that include paralysis, which if left untreated may result in herniation or massive hemorrhage into brain substance.
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" and "without response" to either verbal or physical stimulation: Syncope may occur at rest; with change of posture. 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.
Stupor and coma are characterized by impairment of the arousal system. In stupor, a person arouses only in response to strong verbal or 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.
The ED physician, Dr. 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. From that record it seems clear that the patient had suffered a near fatal reaction to the given medication, as evidenced by the "pupils dilated at approx. 5 mm" with "very little reaction to light", and that 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 edidenced at N-6 of the record between 0030 and 0055 hours, also noted at N-5. That NO bloodwork had yet been done and it seems clear that the ED physician failed to properly assess the patient's condition, which fell far below an acceptable standard of care.
I assume that Dr. Jordan would have been alerted. He 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 of the medical record. Caveat: That he elected to alienate and treat the patient over the telephone, unseen should also be borne in mind.
Further, between 0200 hours and 0220 hours her Blood Pressure had risen slightly from 150/72 to 162/80, a sign of mounting hypertension such as caused or worsened in response to treatment. The record at A-26 documents the time of that assessement as 0220 hours, while N-5 documents the time of the same assessement at 0230 hours.
By 0220 hours the patient's respiration rate was documented as "deep and soaring and without constant jaw thrust", a sign of constriction. The same record at N-5 also documents "gurgly respiration" which can suggest thoracic trauma (seldom occurs as an isolated injury; patients are often in shock) such as associated with the airway and swollowing difficulty in respiratory compromise.
Respiratory depression represents the principal negative variable introduced with conscious sedation and, left unrecognized and untreated, is the cause of most serious complications, including panic.
Panic disorder commonly coexists with essential hypertension and the postural tachycardia syndrome in which blood pressure decreases while heart rate increases. Orthostatic hypotension is a hallmark of diabetic autonomic neuropathy.
The quality of breath sounds may help in determining the level of obstruction. Oropharyngeal obstructions tend to be "gurgly", while laryngeal or upper tracheal obstructions are raspy or stridorous.
The same record documents a HR (Heart Rate) in the 160's with a rapid drop in blood pressure (BP) to 98/70 bpm by 0235 hours.
The earliest indication of shock is an increase in heart rate (HR).
The same record at N-5 documents a physician "assessments unchanged" at the very same time 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 obstruction that occur during sleep, usually associated with a reduction in blood oxygen saturation.
Cheyne-Stokes breathing occurs when there are periods of deep breathing alternating with periods of apnea. A Cheyne-Stokes breathing pattern may be seen in a patient with heart failure, drug-induced respiratory depression, uremia, or brain damage. Conditions that can cause central sleep apnea include poliomyelitis, encephalitis affecting the brainstem, and neurodegenerative illnesses. Evidence of other brainstem malfunction may be seen in the pupils, eye movements and motor and reflex responses.
There are two basic ways in which breathing can stop: directly, by direct drug action on brain breathing centers (particularly in the case of depressant overdoses), or indirectly, by blocking the airway (especially through aspiration of vomitus).
A viral upper respiratory infection is capable of producing airway obstruction. Other causes include panic attacks.
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.
Patients who are unconscious or have signs suggestive of respiratory compromise, however, require immediate attention. It seems clear therefore that the healthcare providers failed miserably to recognise a need for an emergency airway at that time. When a patient is found collapsed or unconscious, there is a real and potential threat of airway obstruction. Without a patent airway gaseous exchange does not take place and hypoxaemia develops.
The evidence speaks when the victims cannot.
Signs and symptoms suggestive or airway or ventilatory compromise include: Breath Sounds
. obtundation 
agitation (which may suggest hypercarbia)
cyanosis
retractions/accessory muscle use
laryngeal trauma
abnormal breath sounds
snoring
stridor - signs of upper airway obstruction are initially those of noisy respiration with stridor
crackles
dysphonia
symmetrical breath sounds over both hemithoraces
tachypnea (rapid breathing)
Presence of stridor indicates critical airway compromise.
N-3 of the record documents "resp noisy", "shallow", "Cheyne-stoke" at 0320 hours. Noise heard during any part of the respiratory cycle may indicate airway obstruction or alteration in airway patency.
The record at N-5 documents the respirations as "deep and soaring with 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.
In this case, inability to establish a patent airway, or purposeful displacement of the endotrachial tube cannot be ruled out.
I had asked the patient twice, in the presence of her foster brother, if she could hear me, and if she could to wiggle her toes and indeed she did, not once but twice, to be absolutely certain, suggests a pseudocomatose state associated with a sympathetic blockade (peripheral vasodilation and hypotension due to sympathetic blockade may occur) , or the product of neuroleptanalgesia, a state of quiescence, altered awareness and analgesia produced by the administration of a combination of a narcotic analgesic and a neuroleptic agent.
In my opinion, Arlene Berry appeared to be more paralyzed or blunted than anything, with the exception of twitching (short spasmodic contractions/retractions of the right leg). 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, narcolepsy, hallmark features of neuroleptanalgesia.
Underlying causes of catalepsy include severe emotional trauma, and emotional shock.
Neuroleptanalgesia is an intense analgesic and amnesic state produced by the combination of narcotic analgesics and neuroleptic drugs. Neuroleptanalgesia is demonstrated by people's ability to acknowledge verbal commands (via auditory stimuli), despite analgesia and CNS depression (Jones and Simmons, 1968). Antipsychotic agents potentiate anticholinergic drugs, and toxic psychosis may occur.
When Dr. Jordan finally showed up in the small hours of May 24, 2000, precious moments that followed were not taken up with measures to save his patient's life, but rather ways to accelerate her demise. He even proposed a "DNR" (do not resuscitate order) and asked us bluntly if we would prefer to "let nature take its course". The family was not impressed. Obviously, Dr. Jordan did not support the use of aggressive interventionist treatment to keep alive someone he had already injured, for to give treatment to remedy a wrong would expose the fact that mistakes were made.
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, indicative of a slow bleeding source in the upper GI tract. 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. Obstruction below the middle of the small bowel also gives rise to brownish vomit. Gastrointestinal or GI bleeding is considered a potential medical emergency. From the record it seems clean that no emergency measures were taken and that the event was met with complete indifference.
The record at N-4 documents "incontinent blood tinged urine" at 0305 hours that is consistent with hematuria (blood in urine), while N-3 of the record documents a "large amount of dilute urine" at 0325 hours, only 20 minutes later, and again at 0450 hours as documented at N-1 of the record.
The record at N-4 documents the patient's "transfer to ICU" at 0320 hours, while record at N-3 documents a "congested oral airway" at the very same time.
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. Further, the patient's condition remained critical throughout the night and into the small hours of the morning notwithstanding. The same record documents a heart rate (HR) of 174 bpm at 0320 hours that is consistent with trauma.
From these records alone 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 that record it seems clear that both doctors should have realized at the onset of severety of the patient's signs and symptoms that they were faced with a critically ill young woman who was not responding to treatment and they should have been acutely aware of the danger. 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.
What I take to be the Ventilation Record at A-17 documents the arrival of the ventilatory therapist, Helene Studholme in the ICU at 0330 hours after being "called in for patient requiring ventilation", while N-3 documents the time of the patient's intubation by Dr. Jordan at 0325 hours, 5 minutes earlier, suggesting that Dr. Jordan intubated the patient unassisted. The same record documents patient "suctioned down ET tube several times for small amount of brownish mucous", a reddish brown liquid, suggestive of old blood or or admixture with blood and gastric content, while A-17 documents the patient as "being suctioned for moderate amounts of coffee-ground emesis by RN" at 0330 hours.
An odorless yellow/brown liquid suggests amebic abscess
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. Suctioning infers that the patient's airway had become obstructed with secretions or debris; complications associated with such negligence include hypoxia, bradycardia, tissue trauma, increase intracranial pressure, and tracheal or pharyngeal perforation.
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. Incontinence is loss of bladder control and is a very serious side effect of antipsychotic medications, such as Stemetil.
During episodes of Hypokalemic periodic paralyses urinary output is decreased during the attack because water accumulates intracellularly in muscles.
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.
A-1 documents "plantars upgoing bilaterally". Submit that plantar reflex is a hallmark of the Babinski sign (a test for signs of disease process in the motor neurons of the pyramidal tract), can result in questionable diagnosis as it is often misdiagnosed. Doctors who cannot distinguish disorders from drug reactions, ie. extrapyramidal side effects are said to be "diagnostically confused", as is the case with far too many northeastern Ontario physicians.
Patients with bacterial meningitis often have a migraine-like headache with severe throbbing, nausea, and photophobia. Spontaneous meningitis can kill in 24 hours if left untreated. Mixed infection can also have devistating consequesces if left untreated with the secondary effect of accelerating death.
The record at N-4 documents the patient's "transfer to ICU" at 0320 hours with a HR (heart rate) of 174 bpm at 0325 hours, notably during the course of the intubation procedure that is consistent with "clinical insult", such as associated with deep pain, or trauma.
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, and again to 85/52 bpm by 3:52 hours, over a span of some 7 minutes, as evidenced at N-2 in the Nurses' Notes
.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". The record at N-3 documents the time of the patient's intubation by Dr. Jordan at 0325 hours, 5 minutes earlier. The same record documents "patient suctioned down ET tube several times for small amount of brownish mucous", while A-17 documents "being suctioned for moderate amounts of coffee-ground emesis by RN" at 0330 hours that is consistent with GI bleeding, a medical emergency that was basically ignored by the healthcare providers.
N-2 of the record documents the ET (endotrachial tube) "pulled back 4 cm" at 0425 hours, the patient having been intubated at 0325 hours. From that record it seems clear that the ET (endotrachial tube) had been malpositioned for one full hour before the error was discovered by one of the nurses, as evidenced by the record, infers a failure of the part of the healthcare providers to identify an incorrectly placed airway. Both myself and the patient's foster brother were present to witness that event. Malpositioning of ET tube can cause airway obstruction and may also result in tissue trauma and bleeding. Pulmonary edema is a well-described complication of upper airway obstruction.
According to my research "when an endotrachial tube is misplaced in the esophagus and misplacement is detected late, a compromise of the patient's safety can be significant". In this case, resulting in a significant loss of cerebral perfusion, including insufficient oxygenation to vital organs. Emesis of reddish brown matter (anchovy sauce appearance) was suctioned from the ETT during and after intubation. Airway compromise can lead to a respiratory arrest. Failure to detect improper placement of anendotracheal tube may lead to pulmonary aspiration which can also be fatal.
Endotracheal intubation (ETI): the insertion of a breathing tube into the trachea (windpipe) of critically ill patients, to maintain the flow of oxygen to the brain and other vital organs. An improperly placed tube or over-advancement of the ETT (for example, in the esophagus) can deprive the patient of oxygen and rapidly lead to death. The full extent of airway compromise may not be evident until 12-24 hours after.
Breathing tube misplacement or dislodgment can result in oxygen delivery to the stomach instead of the lungs, aspiration of gastric organisms into the trachea and the lungs, laryngeal trauma, breathing difficulty and pain; is most likely to occur in those who are neurologically depressed, heavily sedated, or unable to gag. An obstructed airway can be either total or partial and can be recognised by adopting the look, listen and feel approach. In an airway that is partially occluded airflow to the lungs is impeded and characteristic sounds, such as snoring gurgling and/or crowing are emitted. TheMediWeb
N-5 of the medical record documents a “gurgly” respiration’s at 0220 hours.
Gurgling sounds can indicate ET tube placement in the stomach. Gurgling is a bubling sound It usually indicates upper airway obstruction from secretions, emesis, or blood. Gurgling respirations indicate the presence of fluid, usually blood or vomit or both.
Misdirecting the ETT into the esophagus or locating the tip where there is a significant obstruction of its lumen can result in poor ventilation of the patient and eventually lead to cardiac arrest, brain damage or even death. Further, if the ETT is misplaced into a mainstem bronchus, lung rupture can occur. Endotracheal tube (ETT) malpositioning into a mainstem bronchus or the esophagus may result in significant hypoxemia.
Hypoxemia is associated with five basic mechanisms: inadequate inspiratory oxygen, hypoventilation, shunting, defective diffusion pathways in the lung, and ventilation-perfusion inequality.
N-3 of the Nurses' Notes documents a "large amount of dilute urine" (polyuria) at 0325 hours, and again at 0450 hours as evidenced at N-1 of the record that is inconsistent with a documented hematuria (blood in urine), and in particular with respect to the record at A-16, marked by a complete absence of documentation as to water refill to justify urine-output, suggestive of "trauma". In traumatized tissue, bacterium produces many toxins. According to my research, prolonged suction can result in infection if the mucous membranes are traumatized. Further, the coagulation cascade starts when tissue factor is exposed to the bloodstream due to a cut or other injury.
A-4 of the record, what I take to be a Trauma Legend, barely visible in the Physician's Notes, situated at the lower right hand side of that page, there is an obliterated area suggesting perhaps a "white-out", or erasure. Notably, TRAUMA is defined as any insult to the body.
The physician's Lab Work Summary at A-19 documents the charting of a course of HEMATOLOGY and Coagulation. It documents a FIBRINOGEN level of 4.67 H (the normal range is 2.00-4.00). When protein is high, CSF usually clots because of the presence of increased fibrinogen. Serum fibrinogen levels in a safe range is <300 mg/dL. From this record it seems clear that due to Dr. Jordan's mindless and promiscuous use of inappropriate lab settings or other negligence he triggered a Coagulation Cascade of spontaneous slugging of the blood sending numerous "blood-clots", including purulent matter to her brain.
The same record at A-19 documents a D-dimer test level of 1000 H (<500), suggests "thrombosis" (blood clotting). Thrombosis = formation of blood clot(s) 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 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 that is consistent with a systemic inflammatory response to clinical insult, such as caused or worsened by medications, resulting in oxygen deprivation. Pathologic tachycardia accompanies anoxia (lack of oxygen to tissues) as caused by anemia, congestive heart failure, hemorrhage or shock. The same report documents an "inferior ischemia" (decreased blood supply to vital organs). The same document shows ST&T wave abnormalities and abnormal ECG that is consistent with adverse effects of the given drug Stemetil. View Notably, the patient's age was falsely documented at 55 years (she was only 41 years of age).
Hyperglycemia has a deleterious effect on brain ischemia.The Brain is very vulnerable to ischemia due to high oxygen consumption and total dependence on aerobic glucose metabolism.
It is well known that hyperglycemia produces a global decrease in regional cerebral blood flow with a maximal reduction in the BG and leads to alternation of neurotransmitter processing in the BG. After 3-8 minutes without adequate blood flow, irreversable brain injury occurs.
Diabetes harms blood vessels that supply the brain, heart and other organs. Without treatment, pre-diabetes usually turns into full-fledged diabetes.
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, >60 seconds = Panic) and is elevated in 90% of those with coagulopathy, an increased bleeding tendency due to decreased hepatic synthesis of clotting factor, i.e. with prothrombin ( a protein involved in clotting, most commonly prolonged by vitamin K deficiency) The time of that assessment was documented at 0400 hours.
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", clinical manifestations of adrenal insufficiency, or fairly reliable signs of a compromised perfusion. Compare Shock Syndromes in which vasoconstriction, pallor, cold peripheries all point to circulatory failure. Cool, dry skin also suggests late sepsis.
According to the Nurses' Notes at N-1 of the record the patient was given Gravol 50 mg x 10 by paramedics at 0620 hours, while the record at N-7 with respect to medications documents "See Nsg Notes". Notably, Gravol (dimenhydrinate) is contraindicated in chronic lung disease and has also been reported to "mask the presence of underlying organic abnormalities or the toxic effects of other DRUGS" .
Following her transfer to Sudbury on May 24th of 2000, Arlene Berry was was returned to Kirkland Lake several days after family had been notified of her death. Her eyes were sunken in appearance, with swelling and distortion of the face, eyes, and mouth (lips), as was the case, marked by elongated facial furrows (deep wrinkles in the skin) with a rashlike redness resembling a sunburn with significant swelling to the face in the area just below the right eye suggestive of a fixed drug-eruption, or Toxic Epidermal Necrolysis that was evidenced by all who attended Arlene Berry's wake and funeral.
At the first meeting with the coroner held at the OPP Detachment in Kirkland Lake, Ontario in July of 2001, Dr. Barry A. McLellan, the Regional Coroner at that time (now Ontario's chief coroner) admitted to family that there was "no evidence on record to suggest matastasis". At a subsequent meeting between family and the regional coroner, Dr. McLellan provided us with a view of a CT scan that was purportedly done in Sudbury, Ontario just prior to Arlene's death, although I suspect it may have been done several days later. It shows multiple collections of purulent exudates and/or pockets of pooled blood. The enhancement is due to infection.
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. As to the cause of death, according to a Dr. Sauve in Sudbury, she died meeting "brain death" criteria (The first criteria for the determination of brain death were developed in 1968 in part to address concerns that had arisen with the retrieval of organs for transplantation). No pathalogical reason was given. Guillain–Barré syndrome mimicking brainstem death is reported in J Neurol Sci 1993; 120: 115–7.[CrossRef][ISI][Medline]
Metabolic impairment causes demyelination or axonal degeneration. Axonal degeneration secondary to severe demyelination may mimic brain death.
Acute metabolic derangement and endocrine crisis can mimic brain death but more often diffuse cerebral edema, extensive demyelination, or anoxic ischemic injury, is a consequence of these derangements. Examples are brain edema in fulminant hepatic failure and ketotic hyperglycemia. Many severe abnormalities such as hyponatremia, hypernatremia, hyperglycemia or hypoglycemia, hypothyroidism, pan- hypopituitarism or Addison’s disease may decrease the level of consciousness and confound A LESS THAN THOROUGH neurologic examination.
Brain death: resolving inconsistencies in the ethical declaration
Critical illness polyneuropathy is an ICU-acquired condition that affects the peripheral nerves, muscles, and neuromuscular junction. Neurologic crises (polyneuropathy - a reversible cause of paralysis) is associated with prolonged length of ICU and hospital stay and requirement for rehabilitation, with significant use of healthcare resources and cost implications. Neurologic crises may be the beginning of a long-lasting depressive illness followed by arreflexia and acute hypermagnesemia (after use of laxatives), resulting in hypermagnesemic pseudocoma.
"Pseudocoma" (pseudocoma: states resembling acute unconsciousness but with self-awareness preserved) of this kind may be associated with normal consciousness or relatively mild psychological disorders. Most of the cases of this syndrome are caused by basilar artery thrombosis. Further, hypermagnesemia, or hyperglycemia can mimic a variety of neurological symptoms. Many conditions can MIMIC brain death clinically upon examination and without excluding them; you will KILL a person legally despite the reversibility of brain damage. Further, drug intoxication may cause a deep physiologic depression similar to brain death.
Hypermagnesemia causes neuromuscular blockade by inhibiting the release of presynaptic acetylcholine, which results in flaccid paralysis and respiratory paralysis.
Common causes of hypermagnesemia include renal failure and iatrogenic manipulations. Clinically, hypermagnesemia resembles Lambert-Eaton syndrome more so than autoimmune MG. Hypokalemia is implicated as a potential factor in worsening MG symptoms. Acute worsening of MG has been reported following administration of ciprofloxacin, a fluroroquinolone. Hypermagnesemia causes parasympathetic blockade—including cutaneous flushing, hypotension, prolonged QT-interval, delayed intraventricular conduction, respiratory depression, neuromuscular blockade, and coma—and clinically mimics a central brainstem herniation syndrome. 'Symptoms of hypermagnesemia'. Severe hypermagnesemia may mimic brain death. Diabetic neuropathy may predispose
Hypermagnesemia can cause parasympathetic blockade, inducing fixed and dilated pupils, in addition to neuromuscular blockade. Extreme hypermagnesemia can therefore mimic a midbrain syndrome and cause a pseudocomatose state.
IATROGENIC DISORDERS OF THE NEUROMUSCULAR JUNCTION
Anoxic, Metabolic, and Toxic Encephalopathies
Adverse effects are generally associated with hypermagnesemia. Hypermagnesemia may occur during therapy with any bisphosphonate. Sodium biphosphate and sodium phosphate is used to treat constipation. The most common adverse events associated with the administration of bisphosphonates are self-limiting flu-like symptoms related to an acute-phase reaction [28]. See: Rx List
The Clinical Value of the ECG in Noncardiac Conditions
With respect to the initial CT scan hereinbefore 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 because NO biopsy was done. The small lesion, if in fact it is a lesion is also consistant with Occipital Neuralgia, such as associated with headache that can mimic migraine headache (brain tumors, lesions, etc.), which is often misdiagnosed. In the alternative it can suggest demyelination related to a metabolic cause. The bald truth is that localizing signs of brain tumor include a loss of vision on the side of an occipital neoplasm. Compare occipital abscess, a pyogenic brain abscess, usually of bacterial origin.
The lesion in the region of the occipital lobe that measures less than 1 cm seen on the first CT that was done in Timmins is consistent in appearance with an old hemorrhage, or early stage cerebritis during/after capsule formation in the early stage of abscess development (capsules can rupture resulting in the formation of multiple abscesses), or perhaps even an abscess secondary to an occipital dermoid cyst. Rupture of a dermoid and leakage of a cyst contents into a ventricle or subarachnoid space may produce an epidymitis or meningitis respectively. It is contagious and may be caused by viruses, fungi or bacteria. Symptoms may include fever, headache, stiff neck, irritability, sensitivity of eyes to light, confusion, drowsiness or unconsciousness. Death or permanent brain damage may occur if treatment is delayed (especially in bacterial meningitis). Usually full recovery may be expected in 2 to 3 weeks, if there are no complications.
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 this 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. With necrotizing soft tissue infections the expanding lesions would have been asymptomatic (without symptoms).
Even multiple brain abscesses may not cause focal deficit to suggest their presence. It seems clear that was is not a case of metastatic tumor involvement, but rather a clear cut case of abscess formation. Further, with multiple abscesses the meninges typically show a purulent exudate that obscures the sulci making radiographic appearance of microabscesses less visible, hence they are not well opacified. In severe meningitis, the basal cisterns may become completely obliterated and that appears to be what happened here. Morbidity due to a brain abscess generally results from brain herniation due to mass effect, in this case the result of iatrogenic neglect. Further, rapid deterioration is an invariable accompaniment of an untreated condition, in this case pyogenic or purulent bacterial infection.. However, rapid progress of the disease may actually be displaying a pronounced "blood-brain barrier breach", characterized clinically by an abrupt and "rapid evolution", the result of a certain medications which can breach the blood-brain barrier integrity, ie. the drug Stemetil. Breakdown of the blood-brain barrier precedes the inflammatory demyelination.
Reversible demyelination, blood-brain barrier breakdown, and pronounced neutrophil recruitment induced by chronic IL-1 expression in the brain.
Am J Pathol. 165(5):1827-37 - CNS inflammation group
No autopsy was performed. Further, a family request for a formal inquest was also denied. The coroner concluded that Arlene Berry had died of natural causes suggestive of metastatic CA of the brain with multiple brain tumors, after eliciting the opinion of one of his fellow colleagues from the Sunnybrook Health Sciences Centre where he teaches. The medical record of Arlene Berry for May 23rd and 24th of 2000 tells a very different story. In my opinion, Dr. McLellan knowing returned a false finding.
GUILLAIN BARRE SYNDROME (GBS) is a disorder caused by nerve inflammation involving progressive muscle weakness or paralysis, which often follows an infectious illness. Causes of death include adult respiratory distress syndrome, sepsis, pneumonia, pulmonary emboli, and cardiac arrest.
Oversedation may also follow a dose-related extension of the sedative/hypnotic effects of opiates and phenothiazene coadministration. These effects may be indistinguishable from barbituate poisoning. Symptoms include muscle weakness, and extreme somnolence with sedative effects ranging from narcolepsy to lethal catatonia, and acute flaccid paralysis.
Lethal catatonia, a syndrome described several decades before the advent of neuroleptic drugs, has been regarded by many investigators as clinically similar to, and perhaps indistinguishable from neuroleptic malignant syndrome. In fact, NMS has been conceptualized as a "drug-induced iatrogenic form of lethal catatonia".
Neuroleptic malignant syndrome: Definition and Much More From ...
CAVEAT: Neuroleptic malignant syndrome with normal Creatine Kinase is reported in the literature.
Guillain-Barre syndrome is not hereditary or contagious. What causes GBS is a closely guarded "medical secret", highly suspicious for an immune mediated neuropathIic reaction to contraindicated medications, however, in about half of all cases the onset of the syndrome follows a viral or bacterial infection, such as a bout of flu, common cold, or gastrointestinal illness, marked by an infectious process.
A reasonable physician would have correctly diagnosed the patient's condition by doing what Dr. Jordan, including Dr. Spiller and all those who failed to attended to Arlene Berry in a timely manner and/or failed to do in Dr. Jordan's absence. A case of Willful blindness , Criminal negligence , or Mens rea .
In this case, Dr. de la Rocha is suspected of being a carrier of an infectious disease. Further, many immigrant doctors who come to Canada have very low qualifications. Many of them have been exposed to malaria, parasites and unfamiliar infectious diseases, such as amebiasis, a gastrointestinal disease, and also pose public health risks from other emerging infectious diseases. However, about 10% of the world's population is infected with E histolytica, making amebiasis the third most common cause of death from parasitic diseases. Having said that, there is no excuse for misdiagnosis.
When dealing with truth, liars and suppression of truth, or where a crime involves a conspiracy, or conspiracy to cover-up, accuse those guilty of the later freely. They (both those deliberately seeking to lead you astray, and those who are simply foolish or misguided thinkers) generally run for cover when thus illuminated.
The two Cancer QUACKS responsible for Arlene Berry's death
 
Dr. JORDAN, Edward Henry Dr. Spiller, Mark Arthur
...physicians with a propensity for iatrogenic neglect and for 
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, without family consent, and waited for the patient's death.
Further, withdrawing life sustaining treatment from a hyperglycemic patient with concurrent hypokalemia who is under the influence of paralysing agents is of questionable legality. Death results from respiratory paralysis and subsequent asphyxiation. Hyperglycemia and hypokalemia were both present on presentation, but the ED physician neglected to do the bloodwork.
The questionable administration of paralysing agents followed by withdrawal of ventilatory support after ordering it raises more than just ethical issues.
From the record it seems clear that this is a liability murder.
There are four types of crime, as defined in the Canadian Criminal Code, that can be considered murder. or homicide. first degree murder - the intentional killing of another person (1) with premeditation, (2) in the furtherance of another serious criminal offense. (3)manslaughter - the killing of another person where there is no intent to kill . In attempted murder, the mens rea requirement, Latin for "guilty mind", is limited, (4) homicide is when a person directly or indirectly causes the death of another person.
A murder is the the unlawful killing or causing the death of another human being, with malice aforethought. Malice aforethought can be express or implied.
> |
Online