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Cancer Mimics

Arlene Berry died suddenly and unexpectedly at the age of 41, less than 24 hours after being admitted to the Kirkland and District Hospital on May 23rd of 2000. There is a public interest in knowing how Arlene Berry came to her death and how her health care providers are implicated.

Arlene Berry was a robust, strong young lady filled with energy and wherever she went it was like spring, like a breath of fresh air. She believed that fishing was a peaceful means of tackling life's stresses while enjoying quality outdoor time with friends and loved ones. She was an avid fishergirl, hiker, camper, and mother of two (a boy and a girl). Both were only in their early teens at the time of her death.

 

            The Story Behind The Story

This story begins with a trip from northeastern Ontario to northwestern Ontario and a camp out in Thunder Bay District at the Stillwater Creek Tent and RV Park on Highway 17 just west of Nipigon during the late summer of 1998 . The campground comprises 48+ sites, some in wooded area, some along Stillwater Creek and excepting a hiking trail of medium difficulty, is surrounded with pine and other varieties of densely wooded forest. The creek runs through the property crossing under the highway.

One day, while fishing along the trout stream on the other side of the highway, opposite the campground, she had a bad fall in rugged terrain, landing on an old fallen tree stump. The end result, a left sided rib fracture(s). Fractured rib ends can lacerate the pleura or lung, leading to the formation of pulmonary hematomas, hemothorax, or pneumothorax. Rib injuries include bruises, torn cartilage and bone fractures. A fractured rib could easily puncture the lung resulting in partial or complete collapse of the lung.

The primary cause of a collapsed lung is trauma to the chest cavity. The most common mechanism is due to sharp bony points arising from a rib fracture penetrating pleura and damaging lung tissue. Trauma to the chest, such as fractured rib can restrict an individual's ability to breathe adequately. Chest pain and sometimes mild breathlessness are the usual predominant presenting features. Pneumothorax is the collection of air or gas in the space inside the chest around the lungs, which leads to a lung collapse. When the lung collapses, it causes sudden chest pain and shortness of breath.

On rare occasions, the sharp edges of rib fractures have caused aortic lacerations. Chest trauma may also cause a ruptured aorta and even seemingly minor mechanisms of injury can result in rib fracture and aortic laceration. Lacerations resolve more slowly than contusions, and clearance may take weeks or even months, and they usually end in residual scarring and residual masses seen on CT are also scar tissue. Mechanism of delayed aortic injury in left-sided rib fractures have also been reported [Ann Thorac Surg. 2009].

Pneumothorax occurs in about 14% to 35% of rib fractures. Clinical signs and symptoms are nonspecific and include fatigue, weight loss, general malaise, and, less commonly, fever. About one-half of patients remain asymptomatic. Patients with badly scarred lungs, heart or muscle involvement complain of tiredness, fatigue or lethargy due to lack of oxygen and increased work of breathing. Concomitant injuries tend to mask secondary diaphragmatic injury, which along with a delayed diagnosis often cause later symptoms, e.g., .late complications (months to years after injury) such as bowel incarceration or strangulation have also been known to occur

Within a day or so of her injury, Arlene asserted “it feels like air leaking inside of me”. The injury seemingly resolved just as quickly as it appeared with nothing more than a good night's rest and some ibuprofen, a non-prescription NSAID (non-steroidal anti-inflammatory drug) that is commonly used for skeletal pain and inflammation. Notably, a small pneumothorax may resolve on its own and require no specific treatment beyond rest.

Recurrent spontaneous pneumothorax is a disorder often managed by thoracic surgeons. Most etiologies are benign in nature; however, there are several syndromes. Furthermore, delayed pneumothorax occurs in up to 12 percent of patients with penetrating thoracic injuries that initially appear to be innocuous. At any rate, Arlene did not perceive her injury serious enough to warrant medical attention at that time.

Pulmonary fibrosis (scarring in the lung) occurs. Lung scarring is a condition in which lung tissue becomes damaged and scar tissue forms. In time these mature into scar tissue forming permanent adhesions. Sometimes lung scars are small and do not represent a serious problem. In fact, a person may have small or isolated lung scars without even knowing it. On the other hand, large scars or scarring that is spread over a large area of lung tissue can cause breathing difficulties, shortness of breath, and coughing, which may make it hard for a person to do physical activity. Severe scarring (fibrosis of the lungs can also cause respiratory failure.

Pulmonary fibrosis describes a group of diseases which produce interstitial lung damage “mimicking lung malignancy”. What's more, lung infections also mimicking malignancy are not uncommon. A variety of lung infections have radiological features “simulating cancer”. The infections may be fungal, mycobacterial, parasitic or, rarely, viral. Most of these are chronic infections. They do not respond to routine courses of antibiotics. Some of the infections that can trigger lung scarring, according to the Mayo Clinic, include viral infections such as cytomegalovirus, bacterial infections like pneumonia, fungal infections such as histoplasmosis, and certain parasitic infections such as amoebiasis. Amoebiasis in adults in Canada is an unusual disease and although amoebiasis, or the state of being infected with amoeba is rare, it does ocassionally occur

The most frequent cases of pulmonary fibrosis are related to sarcoidosis — fibrosis associated with certain occupational diseases. Pulmonary fibrosis occurs in 20%–25% of the patients with sarcoidosis. It commonly affects young adults,of both sexes, with a preponderence towards people from certain geographical regions, particularly women. Sarcoidosis is a rare disease that results from inflammation. It commonly affects the lungs and skin. It is the most common of the scarring lung disorders. People who have sarcoidosis are predisposed to pulmonary fibrosis (i.e., the hardening and thickening of tissue), although it is not clear if fibrotic processes are active from the onset of sarcoidosis in predisposed individuals, or whether a profibrotic state develops as a response to ongoing inflammation. Furthermore, pulmonary fibrosis has also been known to “masquerade” as metastatic lung cancer

Sarcoidosis is a systemic disorder with a wide variety of clinical and radiologic manifestations. It appears to be more common in cooler climates, but the reason for this is unclear. The disease typically begins between ages 20 and 40. A granuloma forms when an area of tissue within the body becomes inflamed as a result of tissue damage. Granulomas in the lungs is a small region of inflammation due to tissue injury. Granulomas in a lung leaves less space for the air exchange that needs to take place. Granulomas and fibrosis of lung tissue decrease lung capacity and disturb the normal flow of gases between the lungs and the blood. The majority of granulomas are the result of an injury to the tissue, particularly as the result of infection. Sarcoidosis is caused by an overactive immune system allowing inflammation to spread out of control. When found during an x-ray examination, the granuloma is often mistaken for cancer.
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Ninety percent or more of people with sarcoidosis have lung involvement, whether they have symptoms or not. Common lung symptoms are dry coughing, trouble breathing, wheezing, or pain with breathing, chest pain, tightness, or discomfort and occasionally coughing up blood, which is rare, especially in the early stages of sarcoidosis. Many patients with sarcoidosis may also have a “flu-like” syndrome, which may last for weeks or months.
 
Gastrointestinal tract sarcoidosis is rare and may present in the context of generalized disease or as an isolated finding. It may imic other gastric processes, including peptic ulcer disease (PUD), a stomach disorder marked by corrosion of the stomach lining due to the acid in the digestive juices. Manifestations of the disease include stomach pain, nausea, vomiting, and are usually postprandial. Weight loss is common and can be severe, often raising the suspicion of malignancy. Upper GI bleeding can also be the initial presentation, and evaluation often leads to the diagnosis of sarcoidosis. It is not unusual, however, for sarcoidosis symptoms to be more general. Weight loss, fatigue, night sweats,, or just an overall feeling of ill health can also be clues to the disease. Acute loss of body weight reflects loss of fluids and electrolytes and not lean body mass. Enlargement of the salivary or tear glands and cysts in bone tissue are also among sarcoidosis signals.

The stomach is the most commonly affected organ in gastrointestinal sarcoidosis. Gastric sarcoidosis can mimic a malignant lesion owing to narrowing of the gastric lumen or can be revealed by upper gastrointestinal bleeding. Being the “great imitator,” sarcoidosis may mimic a whole gambit of GI processes from peptic ulcers, inflammatory bowel disease, or even carcinomas. Case reports of gastric sarcoidosis are scattered but date back more than 60 years. The lungs are affected in more than 90% of individuals with sarcoidosis. Sarcoidosis is a systemic disease with a 90% predilection for the lungs, but any organ can be involved. Within the gastrointestinal system, gastric involvement is the most common. When this organ system is involved, it can be a feature of systemic disease or an isolated case. Gastrointestinal sarcoid can resemble a broad spectrum of other disease processes; thus, it is important for health care providers to be familiar with the various gastrointestinal manifestations. Patients can have subclinical symptoms or have symptoms of epigastric pain, nausea, vomiting, and hematemesis. Subacute or more rapidly developing symptoms suggest an infectious lesion(s).

Further, gastrointestinal colonic sarcoidosis in association with alternating constipation and diarrhea.has been previously reported on. Over 60 cases of symptomatic gastric sarcoidosis have been described in the literature. A rare entity of gastric sarcoidosis presenting acutely with an upper GI bleed has also been reported. Manifestations of gastric sarcoidosis are usually related either to the presence of peptic ulcerations or to narrowing of the gastric lumen due to granulomatous inflammation and associated fibrosis of the gastric wall. Abdominal pain is characteristically dull, burning, or cramping in nature.

Granulomas are most often found in the lungs and are sometimes mistaken for cancer on X-rays. Two types of common granuomatous diseases are tuberculosis and sarcoidosis. The term granuloma is a medical term that is used to refer to a minute collection of immune cells that are known as macrophages. It is a mass of inflamed granulation tissue from injury or infection, usually associated with ulcerated infections, or invasion by a foreign body. Also, know that granulomatous conditions of diverse etiologies share common histologic features. These granulomatous disorders are often reported as ‘mimicking’ one another. The body may develop a tumor like mass in response to a parasitic infection that is also known as a granuloma, such as amoebic granulomas, an unusual sequelae of amebiasis.

 
http://cogprints.org/7125/1/2010-3-22.pd

"forgotten granuloma" - parasitic


Granuloma may also accompany a parasitic lung infection known as pleuropulmonary amoebiasis. Granulomas may also form around parasites. Regardless of the underlying cause, lung granulomas are not cancerous and most do not require treatment. Treatment may be required if the condition that caused the granuloma is severe or producing symptoms. Musculoskeletal features of sarcoidosis can mimic infection and malignancy. However, sarcoidosis is not related to lung cancer or any other type of cancer or lymphoma.
In this case, while analytic reasoning may suggest pulmonary sarcoidosis, pattern recognition suggests pulmonary amoebiasis, with a mixed picture. Some experts believe that the abnormal immune reaction of sarcoidosis may be triggered by an infection.
The nervous system includes the brain and all the body’s nerves, and it may be affected by sarcoidosis, or amoebiasis. Both of these diseases can cause a mass of granulomas in the brain or meninges, which are the membranes that cover the brain. They also can affect one or more nerves anywhere in the body. Most often, they can also affects the nerves of the face causing one side of the face to droop. Symptoms of disease in the nervous system may vary only slightly for each, or not at all. This may be the first symptom that someone has sarcoidosis.

When sarcoidosis affects the spinal cord, it can cause weakness or even paralysis of the arms or legs. It may affect any cranial nerve, but the most common cranial nerve deficit involves the facial nerve. CNS involvement, with nodular lesions or diffuse meningeal inflammation typically in the cerebellum and brain stem have also been found in every part of the CNS, including the floor of the third ventricle, the occipital, frontal and temporal lobes, etc. have severe headache, nausea, back pain and low grade fever. If the brain is affected, symptoms may include headaches, weaknes.
Sarcoidosis is a systemic inflammatory disease that can affect any organ, although it is often asymptomatic.

Ulcerative colitis is a systemic inflammatory disease that affects many parts of the body. Systemic colitis is inflammation of the colon with additional symptoms outside the colon involving other areas of the body.

Amebic colitis, also known as amebiasis, is a gastrointestinal disorder caused by invasion of the intestine by the protozoan parasite. Protozoa are microscopic Endo and Ecto parasites which serve as Trojan horses for disease-causing bacteria. There are also more severe protozoan infections. The common and well known protozoan infection is amoebic dysentery.
The parasite Entamoeba histolytica causes amebic colitis and systemic amebiasis. Systemic or extra-intestinal amebiasis may develop in 3 months or later after intestinal infection. Up to 10% of the world's population is colonized with Entamoeba histolytica or schistosomal species, thus underscoring the need for effective treatment and public health measures.

An association of ulcerative colitis and histologically proven sarcoidosis has also been reported in the literature. Sarcoidosis is a multisystem inflammatory disease that can also affect the nervous system. Sarcoidosis of the nervous system can also result in seizures, muscle weakness, paralysis of limbs, difficulty in swallowing, dizziness and vertigo. Some of the .symptoms of sarcoidosis are strikingly similar to those symptoms experienced by persons suffering from mold exposure, or perhaps amoebic dysentery.

Past research suggests that sensitivity to environmental factors may be associated with sarcoidosis risk. It is widely believed that sarcoidosis may be caused by a faulty immune response to an inhaled substance. This theory is supported by evidence demonstrating that people who work and live in certain places appear to have an increased chance of developing sarcoidosis, such as people who spend a lot of time around dust, chemicals, and building materials (through their antigenic or adjuvant properties) are all at a slightly increased risk of contracting sarcoidosis. Numerous studies, have observed a predilection for sarcoidosis to become clinically apparent in winter and early spring, peaking in spring months, and variations show higher peaks in winter . If it is assumed that the latency between exposure to the causative agent and development of sarcoidosis related symptoms is in the order of a few weeks to a few months, it seems likely that exposure may first occur in many cases in the late fall to early spring.

Wood smoke, ,such as using wood stoves or fireplaces for home heating may also be a risk factor for Sarcoidosis. The incidence increases in winter through early spring. More than one million Canadian families heat their homes at least partly with wood. Late fall to early spring is the peak time for wood burning, when home heating becomes a factor. Significant air quality problems occur in winter months due to nearby residential wood burning. We smell the smoke in our houses and it irritates the eyes and throat to go outside.

Past studies have also noted a clustering in parts of the country where there is more lumbering activity. In particular, a study by Dunner and Williams suggested that sarcoidosis cases occurred twice as often where lumbering and wood milling was a principal industry. The past sarcoidosis literature should be considered carefully for the possibility that the associations with forests, lumbering, wood milling and wood burning are surrogates for the sensitising antigens they harbour.

It is interesting to note that Arlene Berry had a history of working in and around logging camps in northeastern Ontario. including reforestation activities, such as tree planting jobs, primarily between Matachewan and Kirkland Lake. She was an avid angler and loved fishing and the outdoors, including hunting, camping, and hiking. A hobby included gathering driftwood, pine cones, lichen, and spagnum mosses, as well as various ground pines with resultant exposure to fungal antigens, collected usually in mid fall of the year when high humidity and cool temperatures prevail, and used for creating crafts and curios of all kinds in the final years of her life.

Coexistence of sarcoidosis and malignancy is reported in the literature, but there is nothing on record apart from a paltry CT showing lesions of non specific origin, and a flawed medical opinion to suggest possible malignancy, with absolutely nothing on record to prove it. The original diagnosis of adenocarcinoma was made by Dr. Claudio de la Rocha, an infamous thoracic surgeon, previously convicted of killing an elderly cancer patient he had been treating. He immigrated to Canada from Mexico and is believed to harbour an asymptomatic parasitic disease that affects humans alone and which, especially in its most typical form, suggests an amoebic dysentery.

Acute parasite infection is usually characterized by greater or lesser abdominal distress and diarrhea, and is attended by blood sugar fluctuations, loss of appetite, weight loss, anemia. and tremendous fluid loss. Only rarely is there any visible evidence of infection. Moreover, many laboratories fail to detect the presence of parasites even when presented with specimens from infected persons. Once the condition has moved from acute to chronic, there may be alternating periods of constipation and diarrhea, abdominal distention and bloating, intestinal cramping followed by burning sensations and the sudden urge to eliminate. Generally, there is malabsorption of nutrients, especially fatty foods, irritable bowel syndrome, blood sugar fluctuations, and extreme emaciation. Skin sensitivity is also common: rashes, eczema-like conditions, and even serious eruptions. Many, if not most, parasites migrate so the symptoms could change depending on where the parasites are at any given time, resulting in a patient presenting with a variety of complaints A few patients will have a low-grade fever, anorexia, nausea, vomiting, weakness, and abdominal pain. Fatigue and tiredness are prominent feature in amoebic infection. Physical examination generally reveals little that is unusual. Skin sensitivity is also common: rashes, eczema-like conditions, and even serious eruptions. Amoebae spread by forming infective cysts. About 90% of infected persons are asymptomatic.

There are two basic types of amebiasis: intestinal and extraintestinal disease, which may exist simultaneously. Amebiasis, however, does have some severe forms. These include amebic dysentery and amebic abscesses. Severe forms of amoebiasis include colon ameboma, fulminant necrotizing colitis, and toxic megacolon (a severely enlarged bowel that can rupture). The appearance of symptoms, such as severe dysentery and pain with signs of tenesmus, low grade fever, tachycardia, hypertension, nausea, and anorexia are suggestive of severe forms of intestinal amoebiasis.

http://www.isradiology.org/tropical_deseases/tmcr/chapter1/amebiasisbrain.htm

http://jcm.asm.org/content/49/1/446.full

The most common symptoms of a parasite infection include constipation, diarrhea, gas and bloating, irritable bowel syndrome, joint and muscle aches, anemia, allergies, skin conditions, tumors, nervousness, sleep disorders, teeth grinding, chronic fatigue, and immune dysfunction.

Arlene Berry often complained of aching discomfort in her lower back while living and working as a housekeeper in Red Lake, Ontario, which is usually atypical for people with sarcoidosis. Symptoms may come and go, as they did. This disease is often acute, but in some persons it is chronic, waxing and waning. Extreme exhaustion (not to be confused with muscle weakness ) is one of the more common symptoms of sarcoidosis, however, sarcoidosis can cause muscle pain or muscle weakness.

Sarcoidosis ranks among the top misdiagnosed illnesses and is one of the least understood. It is an inflammatuous disease that can appear in almost any body organ, but most often it starts in the lungs or lymph nodes. It is a type of autoimmune disease associated with an abnormal immune response. The disease can appear suddenly and disappear just as fast. It can also develop gradually and go on to produce symptoms that come and go, sometimes for a lifetime. Tiredness, lethargy, listlessness and joint pains are common. Because sarcoidosis can escape diagnosis or be mistaken for several other diseases, one can only guess at how many people are affected. Sarcoidosis and cancer may mimic one another. and is often misdiagnosed.
Sarcoidosis of the GI tract can resemble malignancy, Gastrointestinal sarcoidosis mimicking colonic cancer is another. Many pathologists will mistakenly classify a biopsy of sarcoid tissue as cancer when it is not. Granulomas are caused by an extremely broad range of disease processes. Other important causes of granulomas are parasitic infections.

https://en.wikipedia.org/wiki/Granulom

Granulomas can appear in the brain, spinal cord and also in the facial and optic nerves. When sarcoidosis affects the brain, stroke-like symptoms may occur. These lesions may be mistaken for primary or metastatic tumors, or tumefactive demyelination.

T-Lymphocytes is responsible for your immediate-response to infection and immune reactions. It is the type type of lymphocyte that functions in cell-mediated immunity that help form the granuloma of Sarcoidosis. Most granulomas in the lung are caused by mycobacterial or fungal infection, but can also be caused by parasites. Fungi may cause a granulomatous meningitis and granulomata or "abscesses" in the brain. The fungal granuloma may also present as multiple brain abscesses. Parasites may also cause brain abscesses. A brain abscess is a focal infection of the brain parenchyma, which may be caused by bacteria, fungi, or parasites.
Further, the coexistence of sarcoidosis and opportunistic infection has previously been documented. In humans, fungal and parasitic infections are usually thought of as opportunistic. Fungi and parasites are especially associated with immuno-compromised patients. The granuloma of sarcoidosis may be formed within inflamed tissue when sufficient lymphopenia-inducing parasites have colonized the monocytes, macrophages and giant-cells in order to sustain a self-activated and non-necrotic inflammatory core . The un-needed T-lymphocytes may then be down-regulated and expelled to the granuloma's periphery, forming the characteristic non-caseating granulomatous pathology of sarcoidosis. Notably, a finding of non-necrotizin granulomas does not exclude an infectious etiology.

Sarcoid granuloma hardly ever form in response to a single species of parasitic lymphopenia-inducing pathogen and the amoebae are no exception. Several parasitic infections can cause granulomas with pathological consequences, which may help explain how sarcoidosis spreads from one part of the body to another.

For the record, 'amoebic granuloma of the lung' has been reported in association with pleuropulmonary amoebiasis. The term "amoebae" covers an enormously diverse group of parasitic protozoans of the genus amoeba or related genera. The possible co-existence of sarcoidosis with amoebae is of interest and suggests a potential etiological relationship. Although non-necrotizing granulomas are the usual finding in sarcoidosis, necrosis can also occur. and is referred to as necrotizing sarcoid granulomatosis. The CT characteristics of necrotizing granuloma are indistinguishable from those of malignant tumors.

Sarcoidosis was once considered a rare disease. We now know that it is a common chronic illness that appears all over the world. Indeed, it is the most common of the scarring lung disorders. Anyone can get sarcoidosis. Females are usually affected more often than males.

The disease typically begins between ages 20 and 40. Notably, pulmonary sarcoidosis can mimic bronchitis, It often goes away by itself, with most cases healing in 24 to 36 months. Even when sarcoidosis lasts longer, most patients can go about their lives as usual. Symptomatic sarcoid myopathy has several forms, the most common of which is a slowly progressive, chronic myopathy, most often seen in post-menopausal women. Sarcoidosis is not a cancer. It is not contagious. Sarcoidosis is currently thought to be associated with an abnormal immune response. Up to 25 percent of those who have undergone either spontaneous remission or resolution of sarcoidosis with or without therapy can have a relapse at a later date.

Notably, sarcoidosis can also show up suddenly with the appearance of skin rashes.(either erythema nodosum, or other types of rashes). On April 13th of 2000, Arlene Berry was prescribed Cortate 1 % CR by her Oncologist, Dr. Hugh Prichard Hydrocortisone topical cream belongs to a class of medications called corticosteroids. It is used to inhibit the function of leukocytes and tissue macrophages, and for temporary relief of minor skin irritations, such as itching and rashes due to a variety of conditions.

Interestingly, the blood of sarcoidosis victims contains a reduced number of T-cells. Spinal cord involvement may present clinically with lower extremity weakness and other nonspecific signs of myelopathy. Nervous system effects such as meningitis, or seizures have been observed, Sarcoidosis is a multisystem inflammatory disease that can affect the nervous system. The Guillain-Barre syndrome is a distinctive neuropathy characterized pathologically by the presence of inflammatory lesions which occur scattered throughout the peripheral nervous system. Sarcoidosis of the peripheral nervous system is reported in PubMed. Sarcoidosis affecting the brain or nerves has been known to occur. Neurologic complications occur in approximately 5 percent of patients with sarcoidosis. Sarcoidosis presenting with an acute Guillain-Barré syndrome has been reported.

http://www.actaneurologica.be/acta/download/2011-1/15-Findik%20et%20al.pdf

In some cases of Guillain-Barré syndrome, the clinical picture resembled brain death. In one report, two cases were presented where the criteria were deliberately misrepresented in an attempt to retrieve an organ for transplantation.
A biopsy is necessary to determine whether a cyst or a granuloma has developed. Both have a similar appearance on a radiograph.

A hallmark of amebic granulomatosis encephalitis is the formation of granulomas around the amoebae. Amoebic granuloma (amoeboma), is also commonly mistaken for cancer. The hallmark of a severe meningoencephalitis associated with numerous parasitic granulomas are well documented. Balamuthia mandrillaris and Acanthamoeba species are 2 free-living amoebae responsible for granulomatous amoebic encephalitis in humans and animals. In Acanthamoeba encephalitis and other systemic infections, the portals of entry are through the respiratory tract and wounds, including surgiccal wounds, with passage to the brain and other sites via the circulatory system. Surgical trauma, burns, wounds, and radiation therapy can also promote infection. The incuba tion period of the disease is difficult to determine, as pulmonary and skin lesions containing the organisms may be present for months before encephalitis appears.The cerebral hemispheres in granulomatous amebic encephalitis may be edematous, with focal cortical softening, hemorrhage and abscesses.

Acanthamoeba sets in with insidious, focal neurologic changes that mimic the clinical picture of single or multiple space-occupying brain lesions. Focal neurologic changes, hemiparesis, drowsiness, personality changes, and seizures are common early symptoms. Headache sets in early and is insidious. Nausea and vomiting may also be early symptoms. Fever is sporadic and generally low. Signs and symptoms of brain parenchymal inflammation develop, such as altered mental status, diplopia, paresis, lethargy, and cerebellar ataxia. The disease progresses over a period of one to several weeks and usually ends in coma and death.

Acanthamoeba can parasitize cutaneous lesions in debilitated patients and eventually disseminate and cause brain lesions also. Acanthamoeba may cause secondary infection in an underlying brain cyst. Sometimes the cysts block the flow of cerebrospinal fluid within the spaces of the brain (ventricles) putting pressure on the brain. This disorder is called hydrocephalus. The increased pressure can cause headaches, nausea, vomiting, and sleepiness.

Presenting symptoms of GAE are nonspecific and can last for months before becoming clinically significant. Once the infection involves the central nervous system, death often results within days to weeks. The course of the disease is insidious and fatal in most cases, mainly due to delayed diagnosis, GAE is an 'opportunistic' infection, usually seen in debilitated, malnourished individuals. Amoebic granuloma can be a complication of chronic infection.

http://path.upmc.edu/cases/case156/dx.html

Could the etiopalhogenesis of granuloma formation in fulminating amebiasis be triggered by Sarcoidosis? Only a small percentage of people have chronic (involving abnormal collections of inflammatory cells) or progressive forms of the illness.

Misdiagnosis of pulmonary sarcoidosis may lead to a greater chance of dying, if not a wrongful death. People with the disease typically develop shortness of breath or a dry cough as inflammation cuts down on their lung capacity. Fatigue, weight loss, and myalgias are also frequently part of the initial presentation. Every year people are diagnosed incorrectly by their trusted physicians. Are you aware that not properly diagnosing a disorder is one of the most universal kinds of medical negligence? It usually begins with failing to take a proper medical history, or lack of diagnostic thoroughness.

CNS sarcoidosis is a rare disorder in which noncaseating granulomas can also affect the brain.

By February of 1998 Arlene Berry had moved back to KL. Her family MD, Dr. Jordan had been treating her assumptively for what he termed to be a “suspected bronchitis”, in spite of enlargement of the distal segments of the fingers, what is known as digital clubbing. Finger clubbing is a thickening of the fingertips that gives them an abnormal rounded appearance. Digital clubbing typically is a sign of underlying disease, usually of pulmonary or cardiovascular origin. Although clubbed fingers are mostly asymptomatic, it often reflects the presence of dreadful internal illness like lung cancer, pulmonary fibrosis, sarcoidosis, or underlying suppurative conditions, e.g. lung abscess.

The following month Arlene Berry was sent to Timmins & District Hospital situated 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”. This refers to residual disease, i.e. cancer cells that remain after attempts to remove the cancer have been made. Chest X-ray showed an area of consolidation; Although it is a general term referring to the accumulation of any foreign substance, "consolidation of the lungs" most commonly infers that an “infection”, or pneumonia, is present. It took another doctor to read her x-ray chart, and to order more appropriate testing before anything was done, which infuriated the patient prompting her to publicly berate her family GP in front of everyone in the ED. According to a hospital insider, she was probably “blacklisted” (alienated, estranged) from that point on, labeled as a "problem patient". Gone was the doctor–patient relationship, gone was the compassion that had once made this hospital a place she could rely on. Blacklisting is multiple providers denying care to a certain patient or patients with a connotation of volition, willfulness, or willful blindness. In northeastern Ontario, this is readily accomplished through a network of providers who share information about difficult, or difficult to diagnose or difficult to treat patients. Launched in March 1998, NORTH Network had been the telehealth organization serving communities in Northern and Central Ontario.
According to correspondence procured by the coroner's office “a diagnosis of adenocarcinoma of the lung was made in December, 1999.

''With respect to neurological function. she remained well until about one week prior to her admission on the 23rd of May. 2000 to the Kirkland and District Hospital. Over that week. she had increasing difficulty walking and tended to fall toward the right side. She developed headaches that became increasingly severe and immediately prior to her hospital admission were associated with nausea, vomiting and drowsiness. The emergency record from the hospital, dated the 22nd of May,2000, documents a history of hematuria for three days and a prescription for treatment for urinary tract infection consisting of Bactrim. The physician who saw her (whose signature is illegible) made adiagnosis of urinary tract infection but considered her past medical history, noting that she had had a left lung resection for carcinoma and that her prior head CT showed no metastasis. He notes, in addition, that she was haqgard in appearance. What I take to be nursing notes, document that she was pale looking and lethargic. From this record it seems clear they recognized that she was sick, but on the basis of the clinical ?ndings at that time, they elected not to admit her to hospital. In my opinion. from the record. there was no indication that she was about to suffer a catastrophic decline”

“You have provided me with a copy of the prior head CT scan that was done on the 16th of March, 2000. The scan was done with iodinated contrast material which makes tumors more visible. In the right occipital region, there is a spot that measures less than 1 cm in diameter that is consistent in appearance with either a small hemorrhage or perhaps a small metastatic tumor. The brain is not signifcantly distorted and the lesion would have been asymptomatic. She returned to the emergency department on the 23rd of May, 2000 with the same complaints. At the time of admission, she was conscious. The triage notes make reference to severe stomach pain, vomiting, hematuria and headache. The time of this assessment is documented as 1705 hrs”.

Although tumor is often the most likely diagnostic consideration in a patient presenting with a contrast-enhancing mass lesion within the brain parenchyma with surrounding edema and mass effect, that is not always the case. Not uncommonly, there can be significant overlap in the radiologic presentation between neoplastic and nonneoplastic diseases. Also know that abscesses or parasites, such as amoeba, may also invade into the brain. At the rear of the brain are the occipital lobes.

For the record, sarcoid lesions have also been found in the right occipital region of the brain, as have 'amoeba-like' spheres mimicking metastasis.

Headache is also compatible with several migraine variants, one of which is occipital neuralgia.

The solitary lesion is also consistent in appearance with a parasitic cyst, or an abscess secondary to an amoebic cyst, or early stage cerebritis during/after capsule formation in the early stage of abscess development.

Often parasites end up in the brain, where they form cysts. Further, a single capsule can rupture resulting in the formation of multiple abscesses. Know that even multiple brain abscesses may not cause focal deficit to suggest their presence, whereas brain tumors are usually associated with multi-focal deficits. Morbidity due to a brain abscess generally results from brain herniation due to mass effect, often the result of iatrogenic neglect, or substandard care, or both.

Also know that neurosarcoidosis may manifest itself in many different ways. It may appear in an acute explosive fashion or as a slow chronic illness. Furthermore, any part of the nervous system can be attacked by sarcoidosis, but the cranial nerves, hypothalamus and pituitary gland are more commonly involved. Sarcoid granulomas can affect the meninges, parenchyma of the brain, hypothalamus, brainstem, subependymal layer of the ventricular system, choroid plexuses and peripheral nerves, and also the blood vessels supplying the nervous structures. Neurosarcoidosis is slightly more common in women than men. One-third of neurosarcoidosis patients show multiple neurological lesions. Most patients with peripheral neuropathy from sarcoidosis also exhibit other systemic or CNS manifestations of the disease. Further, a biopsy is required for obtaining tissue for pathological confirmation of the diagnosis.

Although a diagnosis of adenocarcinoma of the lung was made in December. 1999, one might wonder if Arlene Berry really had lung cancer in the first place. The pathology literature is replete with reports of benign entities mimicking lung carcinoma. A malignant diagnosis cannot be made with a reasonable level of certainty. There is a multitude of ways in which lung cancer can be underdiagnosed, overdiagnosed, or misdiagnosed. “Pseudomalignancies” of the lung fall into 2 general categories: reactive processes misinterpreted as cancerous and benign tumors mistaken for malignancy. Mistaking reactive atypia in the setting of pneumothorax for adenocarcinoma is such an example (a wide variety of pulmonary and pleural histological changes is recognized in the setting of spontaneous pneumothorax). Others include: primary or multiple pulmonary amyloidosis mimicking metastatic lung cancer lesions; pulmonary hyalinizing granuloma (a benign entity of unknown origin) presenting with a central mass in the left lung mimicking lung carcinoma that is frequently mistaken for metastatic carcinoma radiographically; pulmonary sarcoidosis; and fungi can also masquerade as primary or metastatic lung carcinoma (also reported in the literature), and myriad more. A broad spectrum of nonneoplastic conditions can also mimic a brain tumor, both clinically and radiologically. Conditions such as brain abscesses, granulomatous conditions and focal demyelination may mimic brain metastasis in their clinical and radiological manifestations leading to misdiagnosis, as in this case.

A common dilemma encountered in the outpatient primary care setting or in the hospital is the finding of an abnormal lung mass on a routine chest film. Because the leading cause of pulmonary nodules is lung cancer, look-alike infections are often diagnosed incidentally during the evaluation of a presumptive malignant process. Adenocarcinoma, the most common type of lung cancer, is usually located on the outer surface of the lungs (periphery) and can be mimicked by pulmonary sarcoidosis.

Sarcoidosis or sarc is a multisystem disorder characterized by granuloma, ball-like encapsulations of phagocytic cells driven by microbes. Sarcoidosis is often called the “great masquerader” as there may be several atypical or nonspecific presentations – including not just the lungs but the brain, lymph glands, spleen, liver, skin and heart among others. Furthermore, pupillary abnormalities, including internal ophthalmoplegia have also been described in sarcoidosis.

An infectious etiology of sarcoidosis has long been suspected. Today scientific evidence provides a strong, if not conclusive, link between infectious agents and sarcoidosis, and parasitic agents are no exception.

On or about January 13th of 2000, Arlene Berry was admitted to the Timmins & District Hospital in Timmins, Ontario, where a left pneumonectomy was performed under the care of Dr. Claudio de la Rocha, a cardiovascular and thoracic surgeon who immigrated to Canada from Mexico. Following surgery, Arlene Berry was discharged home 5 days later. An early hospital discharge can either suggest a cost driven premature discharge, or portend a low risk with a reasonably favorable prognosis. As health insurers look to cut the costs of patient care, one of the most frequent (and dangerous) tactics they sometimes adopt is discharging patients too early from the hospital or other site of care. Surgery for patients who have had the left lung removed is generally between 96% and 98%.

On or about March 16th of 2000, Arlene Berry returned to Timmins where she underwent follow-up study and testing at the same hospital, consisting of a CT scan, and a mediastinoscopy as part of her post-operative evaluation. Mediastinoscopy is carried out in hospital, under general anaesthetic. If you are having a mediastinoscopy, a small cut will be made at the bottom of your neck, usually in the normal skin folds. A mediastinoscope is inserted through the incision. Possible complications linked to the procedure include haematoma (a collection of blood, usually clotted), injury to the esophagus or voice box (larynx) with change in voice quality for some time, and infection at the site of the procedure.

What the family had found to be peculiar, was a dramatic voice change following the mediastinal procedure, suggesting a “partial vocal fold paralysis”, or decreased vocal fremitus, now believed to have been procedure related. Gone was her distinctive, naturally “raspy” voice. Although Arlene began to regain her voice in the weeks that followed, her voice remained somewhat “whispery” (speech volume was low) for the remainder of her days.

According to the Outpatient record at OP-54, the patient’s recent head CT scan showed “NO METASTASIS”, and her mediastinoscopy, a surgical procedure to examine the mediastinum inside of the upper chest between and in front of the lungs, were found to be “NEGATIVE”. A normal result for a mediastinoscopy means no abnormal tissue, growths or signs of infection are present at the time. From that record it is clear that NO clinically detectable metastasis were found. Metastasis is the process that involves the spread of a tumor or cancer to distant parts of the body from its original site. Mediastinoscopy remains the “gold standard” to evaluate abnormal mediastinal lymph nodes. For mediastinal lymph adenopathy of diverse etiologies, mediastinoscopy is diagnostic in 97% of reported cases (Gossot D, Toledo L, Frisch S, et al). The high yield reflects the generous volume of biopsy material obtainable with this technique.

Following that testing, Arlene Berry confided “I don’t have AIDS, or brain tumors, or anything like that, but I might have a cyst, or infection”, and elaborated on how “some people could be carriers and not even know it”. It would have been an incidental finding, acquired in hospital and which was not present initially at admission,while under the care of Dr. De laRocha. Some cysts can remain viable for up to 4 months or longer. Detected March 16th of 2000, with a timeline between January 13th and March 16th, postoperative. A condition is considered to be asymptomatic if it fails to show the noticeable symptoms with which it is usually associated. Iatrogenic (doctor caused) infection is influenced by factors like poor sanitation and hygiene, e.g., external inoculation with contaminated hands, surgical gloves, instruments (such as insertion of a bronchoscope into the lung through the mouth), etc. resulting from medical treatment or surgical procedures cannot be ruled out.

Most people tend to think of cysts as entities encountered frequently in derma-tological clinics. A cyst is a closed pocket or pouch of tissue that can form anywhere in the body. Most are asymptomatic and cause no real issues.

Parasitic infections can manifest in many different ways, from calcifications to cysts, and are based on the type of infecting parasites present. Parasites may cause acute meningitis or encephalitis, chronic encephalopathy, and cerebral granulomas.  

The word cyst is derived from the Greek word kustis, meaning ‘bladder’. A cyst is a suitcase for the material inside. Cysts can be congenital but are usually acquired. Some of them relatively harmless, and some of them trojan horses of the potentially lethal variety. There are many conditions in which lung cysts develop, but in most cases, they are not cancerous. Occasionally, cysts can be related to cancer, but cancer is not associated with an assymptomatic carrier state because cancer is NOT contagious or transmissable. There are many conditions in which lung cysts develop, but in most cases, they are not cancerous.

Google search terms: cyst, infection, asymptomatic carrier = “amoeba”. The parasite can cause ulcers to form in the intestine resulting in amoebic dysentery. Amoebiasis is both infectious and transmissible by direct or indirect contact and sooner or later follows the fulminant progress of a potentially lethal opportunistic infection requiring emergent management that, unless diagnosed and treated in a timely manner, can kill within hours or days once symptoms appear. Cysts are typically resting, dormant and/or resistant stages in the full life cycle This parasitic disease primarily affects people who have been ill for quite some time, or those with a weakened immune system. Parasites sap our strength and weaken our immune system. They steal nutrients from the food passing through our GI tract and leave us malnourished and sluggish. Constitutional symptoms, such as low-grade fever, fatigue, malaise, or anorexia, are nonspecific and can be mild or severe.

http://healing.about.com/cs/uc_directory/a/uc_parasites_2.htm

Cyst formation is triggered by the dehydration of gut contents in asymptomatic carriers. Parasites (and toxins) in the intestines can sometimes enter the blood and be carried to the organs and tissues of the body, including the brain, and here's the kicker: Parasitic cysts of any origin may mimic primary or metastatic brain tumor(s). The pressure exerted by the growing cysts can cause paralysis or brain damage, or even blindness. Sometimes the cysts block the flow of cerebrospinal fluid within the spaces of the brain (ventricles) putting pressure on the brain. This disorder is called hydrocephalus. The increased pressure can cause headaches, nausea, vomiting, and sleepiness.

Arlene Berry was then referred to the Northeastern Ontario Regional Cancer Centre situated at the Laurentian Site, Sudbury, Ontario for consideration of radiation therapy under the care of Dr. Hugh Prichard, a radiation oncologist. It would have been about the last week of March of 2000. While receiving treatment in Sudbury she stayed at the Daffodil Terrace Lodge, where, between appointments, she spent her leisure time fishing off the shores of Ramsey Lake. The treatment lasted about 5 weeks. During that time, she remained quite well. Except for skin rash – see Rx Skin sensitivity is also common: rashes, eczema-like conditions, and even serious eruptions.

By the end of April of 2000, she had completed her post-operative course of radiation therapy. In light of this treatment, her condition was seen to be stable. She was dischared home to Kirkland Lake on or about the last day of April, 2000. She had been scheduled for an x-ray follow-up in Sudbury on Tuesday May 30th at 2:30 PM. Sadly, she did not live long enough to meet this appointment. Ontario's healthcare system had failed her.

What now also concerns me is the normal result for the mediastinoscopy done on March 16th of 2000, meaning no abnormal tissue, growths or signs of infection were present at the time. The detected cyst would have been dormant, in other words an infection waiting to happen. This was not cancer and the doctor not only identified finding a cyst with which he himself was familiar, he subjected his patient to unnecessary radiation rather than admit he screwed up and knowing that the cyst, once unleashed was going to be the death of her.

Arlene Berry remained quite well untill the last week or two of her life. Within two weeks following radiation therapy she developed flu-like symptoms suggestive of gastrointestinal illness. It began as an upset stomach with nausea. She had also noticed increasing weakness of her legs, and two weeks before her final admission she had developed flu-like symptoms. Then began the abdominal pain and bouts of diahrea with alternating constipation progressing to bloody stools that was accompanied by headache, vomiting and general feeling of malaise. By this time she had lost her apetite and developed a serious aversion to food. She thought she had the flu due to an associated achy feeling. She felt she might be developing an ulcer, such as a peptic ulcer and so took the odd drink of buttermilk, which wasn't very well tolerated due to nausea.

All ulcers of the stomach or intestine can cause nausea and vomiting, upper abdominal pain, loss of appetite, weight loss and bleeding.– the symptoms are quite similar for all types of ulcers. Patients with ulcerative colitis present with some combination of diarrhea, bloody stools, and abdominal pain.

Flu-like illness is also a common complication of radiation therapy which results from radiation injury of the CNS, and may include ischemia and necrosis. and the very same flu-like symptoms are followed by slurred speech and loss of consciousness in humans affected by amoeba, Diarrhea is usually present; however, the patient can be constipated.

Google search terms: ulcers, cyst, asymptomatic carrier = Amoebiasis

Interestingly, iatrogenic lymphocytopenia is caused by either cytotoxic chemotherapy or radiation therapy, or both, 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 number of lymphocytes declines within the first 12 to 48 hours after exposure. This is followed over several weeks by a decline in the number of other blood cells. The decline in lymphocytes is one of the best early signs of the severity of the radiation injury. Radiation therapy, in this case, is undoubtedly the cause of immunosuppression and an increased susceptibility to invasive bloodborne carriage of infection.

Over the last week of her life Arlene tended to become somewhat confused and easily irritated. She developed muscle weakness, difficulty in walking, facial weakness (evidenced by a crooked smile), slurred speech and drowsiness progressing to extreme fatigue.

Extreme exhaustion is one of the more common symptoms of sarcoidosis. When bilateral facial nerve palsies develop in young adults, sarcoidosis is the most likely cause. Drooping of one side of the face results from sarcoidosis affecting a facial nerve. This can be confused with Bell's palsy, a disorder that may be caused by a virus. Central nervous system involvement by sarcoidosis (also termed neurosarcoidosis) is relatively common among patients with systemic sarcoidosis and has a bewildering variety of manifestions. Sarcoidosis is a systemic disorder characterized by non-necrotizing granulomatous inflammation, with varying degrees of concomitant fibrosis. Neurosarcoidosis is a complication of sarcoidosis in which inflammation occurs in the brain, spinal cord, and other areas of the nervous system. Slurred speech, impaired swallowing, hoarseness, and central nervous system involvement may also be noted. Gastrointestinal tract involvement has a prevalence of less than 1% and is usually associated with pulmonary involvrment.

Sarcoidosis disease and brain damage are interlinked as well, which is when the granulomas appear in the meninges of the brain, which is the protective membrane that shields it. Granulomas are the pathologic hallmark of sarcoidosis. Granuloma is an organized collection of macrophages. One of the most aggressive manifestations of these disorders is the encephalitic form of the disease. The encephalitic form means that there is inflammation of the brain parenchyma; that is in contrast with other forms of the disease, in which the inflammation is predominantly the meninges, the covering of the brain. These forms may affect white matter, grey matter or it may produce tumor-like lesions. Meningitis may involve the brain stem which would contribute to cranial nerve involvement and subsequent cranial nerve paralysis. Meningitis can strike in an instant. In very aggressive forms, the patient may manifest with a thickening of the dura mater or even the presence of tumor-like lesions of the dura mater that often mimic brain tumors. The granulomas of sarcoidosis can have a severe impact on the brain leading to death if left untreated, or inappropriately treated.

The outpatient record seen at OP-53 documents a 4 day history of bloody bowel movements (bloody stool) when voiding, evidenced by “bloody BM’s x 4 days”, can suggest a parasitic etiology. This can also be an indication of chronic or even severe amoebiasis. The same record documents that she was “pale-looking and lethargic”, and also that she had been taking Tylenol and Aspirin, noting "daughter states takes a lot", suggests a history of over-the-counter medications that can break the gastric barrier and damage the gastric mucosa (lining of the stomach).

Constant tiredness and fatigue manifest the symptoms of lethargy. Palor and lethargy are suggestive of anemia and indicate the need to perform blood tests. Parasitic infections are important causes of anemia, usually overlooked. Parasite infections generally receive less attention than other diseases. Lethargy and drowsiness are often also associated with moderate to severe dehydration, including congestive heart failure. Lethargy may also be caused by the toxic effects of waste products on brain function.

All ulcers of the stomach or intestine can cause nausea and vomiting, upper abdominal pain, loss of appetite, weight loss and bleeding.– the symptoms are quite similar for all types of ulcers; Ulcers and inflammation of the inner lining of the colon can also lead to symptoms of abdominal pain, diarrhea, and rectal bleeding with ulcerative colitis. The term “ colitis” is non-specific and refers to any inflammation of the colon. Bloody diarrhea. the hallmark presenting symptom of UC (ulcerative colitis) is mimicked by infectious dysentery. Typical symptoms of amebic colitis are diarrhea and rectal bleeding.

The record at OP-53 dated May 22nd of 2000 documents a recent history of urinary-(tract infection, evidenced by “Here 1 week ago for UTI. Last period on 6th of May”. followed by a more recent history of “hematuria” (blood in urine) for “three days”, seen at OP-54. The healthcare provider who saw her made the diagnosis of UTI. The same record documents a prescription for Cipro, for treatment of urinary-tract infection. The belated test result evidenced at OP-55, later returned a finding of “NO Growth”. Routine bacterial cultures are usually NEGATIVE for pathogens, showing “No Growth”, however, a negative urine test can also suggest the presence of unusual bacteria, or viruses causing symptoms of UTI. Although Escherichia coli (also called E. coli) bacteria cause the majority of UTI's, many other bacteria, fungi, and parasites may also cause UTI's.

Although UTIs are almost always caused by bacteria, some viruses, fungi, and parasites can infect the urinary tract as well. Parasites can also live in the vaginal area where they can cause yeast and keep it there. They can cause itching and inflammation by directly attacking the mucus lining of the vaginal area. Parasitic infection symptoms that lead to recurring yeast infections include abdominal distress. Not all fungi are yeasts. There are both parasitic fungi and parasitic yeast, based on the nature of their behavior in the body. Although rare, parasites can and do cause urinary tract infections. It is very unlikely that a GP will ever tell you that the cause of your illness is related to parasites. And the fact that GPs never even test for these inhabitants is proof of negligence.

Onset of menstrual period as evidenced at OP-53 is closely related (within time frame) to illness in which symptoms of UTI result from production of toxin which may then wash backwards up through the vagina, uterus and fallopian tubes (or similar mechanism associated with toileting) to be absorbed from the colon.

http://www.ehow.com/about_5384343_amoebic-dysentery-symptoms.html

There can be many complications of urinary tract infections, including dehydration, sepsis, kidney failure, and death. You are more likely to develop a urinary tract infection when you are dehydrated. Dehydration can also cause the symptoms of the urinary tract infection to appear more severe; loss of fluid and sodium takes a toll.

OP-53 documents “For 2 weeks had flu, migraines”, while A-5 of the record documents the presenting complaint as “headaches”, accompanied by “severe stomach pain”, and “abdominal pain ongoing for 2 weeks”. Migraines can be associated with certain gastrointestinal problems. Abdominal or stomach pain concurrent with nausea and vomiting points to the abdomen as the source of the problem. Nausea and vomiting are common features of many GI infections. A headache that is present with an intestinal infection may also indicate signs of dehydration, which should have been a 'red flag' suggesting the possibility of intestinal obstruction, or pseudo-obstruction which represented a potential emergency..

Transitions from one type of intestinal syndrome to another can occur and intestinal infections can give rise to extraintestinal infections.

According to the record at A-6, she returned on May 23rd to the ED (emergency department) “with the very same complaints”. Know that rapid evolution of illness and patient return within 24-48 hours suggests a severe illness. The healthcare provider who saw her noted that she had been “taking morphine” for pain management, and also that she had recently “stopped” taking the morphine, evidenced by “stopped this week”, noting her recent medical history and that for “2 weeks” she had the “flu”. The same record also documents a question mark (?) with respect to possible morphine allergies, evidenced at A-5. Sudden opiate withdrawal (quitting cold turkey) leads to a syndrome called opiate withdrawal syndrome. Opiate withdrawal (as opposed to a proper taper) refers to the wide range of symptoms that occur after stopping or dramatically reducing opiate drugs after prolonged use (several weeks or more).

Opioid-withdrawal syndrome also resembles a severe case of influenza; symptoms peak at 72 to 96 hours but last for 14 days or more. In addition, the symptoms include agitation, anxiety, depression, muscle aches, pupillary dilatation, abdominal cramping, and diarrhea. Complications include nausea, vomiting and breathing in stomach contents into the lungs. This is called aspiration, and can cause serious infection. Vomiting and diarrhea can cause dehydration and body chemical and mineral (electrolyte) disturbances. Opiate withdrawal can result in death for unhealthy patients.

The biggest complication is return to drug use. Most opiate overdose deaths occur in people who have just withdrawn or detoxed. Because withdrawal reduces your tolerance to the drug, those who have just gone through withdrawal can overdose on a much smaller dose than they used to take. In this case, Arlene Berry was given 30 mg morphine sulfate, after several days withdrawal. The physician who cannot tell that his drugs are producing ill effects upon his patient until serious, even fatal consequences evolve, has no business dispensing drugs.

Rapid i.v. injection of the drug may result in opiate-induced adverse effects; severe respiratory depression, apnea, hypotension, peripheral circulatory collapse, chest wall rigidity, cardiac arrest and possible anaphylactoid reactions. Overdosage with morphine is characterized by respiratory depression (a decrease in respiratory rate and/or tidal volume, Cheyne-Stokes respiration, cyanosis), extreme somnolence progressing to stupor or coma, skeletal muscle flaccidity, cold and clammy skin, and sometimes bradycardia and hypotension. In severe overdosage, apnea, circulatory collapse, cardiac arrest and death may occur.

MORPHINE SULFATE INJECTION BP - RxMed

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 enemas to assist with stool evacuation, and also due to dizziness, marked by a sense of uneasiness progressing to unsteadiness. A question of GI motility? Resulting decreases in GI motility from antidiarrheal medications may cause constipation and bowel obstruction. Further, constipation as an adverse effect of opioid use is almost universal: “In one study, 95% of patients interviewed by nurses in a hospital oncology unit reported constipation as the major side effect of their opioid pain-control regimen. Monitoring should have began with a thorough history of the patient's bowel habits before starting opioids and stemetil. Phenothiazine compounds should not be used in patients receiving large doses of hypnotics (opioids), due to the possibility of potentiation.

Enema is contraindicated in patients with fulminant disease, because of the danger of precipitating toxic megacolon or perforation of the colon. I know for a fact that she had been severely constipated at one point and that “megacolon” was a factor. Toxic megacolon is a well known complication in inflammatory bowel disease such as ulcerative colitis, Crohn's disease, or Sarcoidosis.

http://pmj.bmj.com/content/62/727/341.full.pdf

The development of toxic megacolon as a complication of infectious colitis is rare. However it is recognised as a complication of enteric infections caused by Clostridium difficile, Campylobacter jejuni, Shigella, Salmonella species, Cytomegalovirus and amoebae. Toxic megacolon is the clinical term for an acute toxic colitis with dilatation of the colon. The term "toxic" means that this complication occurs with infection or inflammation and is very dangerous. A physical exam may reveal signs of septic shock.

Toxic megacolon can complicate 5% of cases with severe IUC. It can also be triggered by hypokalemia, NSAIDs use, colonoscopy, infection with CMV, amoeba or C. difficile (both conditions can co-exist), and indiscriminate use of opiates, which are known to precipitate toxic megacolon (exacerbating factors include narcotic and anticholinergic medications). Physical examination may reveal a toxic appearing patient with altered sensorium, tachycardia, and fever that may be low grade. Vague abdominal pain may be present but is not the most prominent symptom. A preceding history of diarrhea, bloody stools, abdominal pain, chills, anemia, and clinical deterioration may ensue. Signs & symptoms of shock (such as tachycardia, breathlessness and decreasing level of consciousness) are a common findings in parasitic infection, usually the result of cardiac tamponade, Pain, cardiac tamponade, and sepsis are the most common clinical findings .

See signs of systemic toxicity in megacolon: Any 3 of the following - Fever (>101.5°F), tachycardia (>120 beats/min), leukocytosis (>10.5 x 103/µL), or anemia; Any 1 of the following - Dehydration, altered mental status, electrolyte abnormality, or hypotension.

According to Dr. Jordan, “she had presented to the ED several days before with vomiting and it was thought that she had a UTI”, to rule out delay in seeking treatment. According to the hospital record at A-8 “she was given antibiotics and sent home”. This is a common ploy used by doctors and hospitals when it comes to to evading emergent complaints. The Victorian Order of Nurses (VON) had to be contacted in order to get her admitted to hospital in the face of life threatening indicators. VON is Canada's largest, national, not-for-profit, charitable home and community care organization.

According to the hospital record seen at A-6, Arlene Berry was admitted to the Kirkland and District Hospital on May 23rd of 2000 by a Dr. Spiller for “IV fluid and Gravol”. According to the same record, she was admitted for “vomiting”, not a diagnosis, but rather a symptom of many causes. Diagnosis involves detailed assessment of medical history of the person, Clearly, Dr.Spiller (the admitting physician) failed in his duty to perform a careful evaluation of the patient's medical history and symptoms.

Dehydration is the main concern with most vomiting. If the symptoms continue for days, they are usually considered severe. Further, a prolonged bout of diarrhea or vomiting can cause the body to lose more fluid than it can take in, resulting in dangerous dehydration. Loss of appetite and fatigue are early signs of dehydration. Dehydration is the most common general complication of intestinal parasite infections. Symptoms of dehydration include headaches, dry skin, palor, lethargy, mood changes and slow responses, dark-coloured urine, weakness, and tiredness.

What appears to be a referral at A-6 of the medical record, a chart-copy from the admitting physician (Dr. Spiller), directed to the attention of the family physician (Dr. Jordan), documents what I take to be a provisional diagnosis of “vomiting”, and “vomiting, lung CA”, suggests a failure or reluctance on the part of the ED physician to adequately diagnose, as evidenced by his perfunctory (careless, indifferent) examination. seen at A-11. I take the record very seriously and he clearly did not. He missed the obvious signs of comorbidity (existence of more than one disorder at the same time ) because he declined to look past the symptom of “vomiting”, and so made an assumptive diagnosis of “vomiting, lung CA”. If you start from a wrong assumption, you end up with a wrong conclusion.

The Health Management Record seen at A-21 documents the patient’s sensory cognitive perceptual pattern as “sedated”. Sedation is the depression of a patient's awareness to the environment and reduction of his/her responsiveness to external stimulation. For the record, electrolyte derangements can mimic sedative intoxication. Sedation can cause both hypertension and hypotension.

The record at OP-54 dated May 22nd of 2000 documents “large blood trace leukocytes”, what are an unusually high number of white blood cells. The presence of white blood cells in the urine usually signifies a UTI; hematuria may also be noted. The presence of leukocytes in urine is referred to as pyuria (pus in the urine). Urinary tract infections due to leukocytes in urine are more common in women and the conditions can vary from cystitis (an inflammation of the urinary bladder) to severe infections of the kidneys or bladder. The record at OP-54 documents “SEPTRA DS GIVEN BEFORE & CIPRO GIVEN AFTER”.

Cipro is a broad-spectrum antibiotic indicated in the treatment of a variety of infections, including UTI. Bactrim/Septra DS is also the antibiotic most frequently associated with drug-induced aseptic meningitis. The same healthcare provider (whose signature is illegible) also made a notation with respect to the “flu”, which was then directed to the attention of the patient’s “family MD”, namely, Dr. Jordan.

OP-54 also documents a “haggard appearance”, usually the result of a long, harrowing or emotional ordeal, The bald truth is that this patient appeared more anemic and dysthymic, thin and undernourished than anything else. Futher, weakness of facial muscles produces a characteristic haggard appearance, or a deceptively disinterested facial expression. The characteristic appearance of a “haggard” or “mournful” face and drooping eyelids is caused by facial muscle paralysis. A sagging mouth or a crooked smile is a part of the same problem.

N-9 of the nurses’ notes documents a PRECAUTION for a “resistant bacteria”, 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 seen at A-21. There are no further details, suggestive of deliberate omission.

At the time of her admission to the Kirkland and District Hospital, Arlene Berry’s blood pressure was documented at “115/70 bpm, with a pulse of 79 and regular”, as evidenced at A-6. Normal blood pressure is defined as a systolic (top) pressure of less than 120 mmHg, and a diastolic (bottom) pressure of less than 80 mmHg The same record documents “mild diffuse weakness” and “difficulty ambulating”, including a respiratory rate of 18, on admission. The normal adult respiration rate is 12 to 18 breaths per minute. At the time of this assessment (18:45 HOURS), Arlene Berry was found to be “alert and oriented”, with “NO Focal deficits”. .Further, the patient's weakness best fits with a process affecting the muscles. There are numerous etiologies for muscle weakness, including infectious, metabolic, autoimmune, endocrine, and toxicologic causes.

http://www.emedmag.com/PDF/043120022.pdf

The word "diffuse" means "widespread" and refers to symptoms that are not localized to just one or a few areas. Instead, it is more or less all over, or at least in many areas.. Many patients report weakness when their problem is fatigue. Weakness and fatigue are terms that are often used as if they mean the same thing, but in fact they describe two different sensations.

Fatigue is a feeling of weariness, tiredness, or lack of energy. Fatigue (also called exhaustion, tiredness, lethargy, languidness, languor, lassitude, and listlessness) is a subjective feeling of tiredness which is distinct from weakness, and has a gradual onset. Fatigue or extreme tiredness are common features of parasitic infection. Diffuse weakness may result from polyneuropathy, myopathy, neuromuscular junction disease, or systemic fatigue. For the record, sarcoidosis can also present with slowly progressive diffuse weakness.

The emergency department record at A-6, what I take to be Dr. Spiller’s physical examination, documents a “soft, non-tender” abdomen, and “no masses”, suggests a typical admitting physical note to express an overall, normal, negative abdomen. A normal abdomen is soft and non-tender. A negative finding can also suggest hypotonia, a disorder that causes low muscle tone that results in muscle weakness. Hypotonia is often the presenting sign for many systemic diseases and diseases of the nervous system. The abdominal muscles feel ‘soft and doughy’; also a sign of gastropareses in clinical diabetes, which can rapidly progress to intestinal obstruction. Delayed diagnosis invites tragic consequences.

On examination, the physician who saw her documented positive “bowel sounds”, evidenced at A-6. Hyperactive “bowel sounds” provide the most immediate indication of persistent upper GI bleeding/GI hemorrhage. An accompanying crampy abdominal pain can also suggest acute bleeding. Fatigue, shortness of breath, lethargy and pallor may also be noted. Gastrointestinal bleeding ALWAYS requires prompt physician evaluation.

A-23 documents a “slurred speech” as evidenced by a ? in the upper left corner of that document, suggestive of systemic toxicity, ie., the toxic effects of a life-threatening bowel disorder. Slurred speech can be caused by disease or damage affecting the muscle and nerves of the vocal cords, The symptoms of a brain abscess include slurred speech. In the majority of cases signs and symptoms continue for no more than two weeks before the patient is hospitalized, as in this case.

Arlene Berry was still neurologically responsive when I saw her following her admission. She was able to reach and use for herself the kidney basin at her bedside table, as she occasioned to vomit more of the same flu-like “yellowish liquid” that she had done so many times on the days before, and in fact used it for herself in family presence, at which time a cool cloth was provided by the nurses, as evidenced by the record 'family in” seen at N-6. The same record documents upwards of “100cc yellowish fluid”, what I take to be frank bile, or ‘bilious vomit’ (toxic chemicals removed from the blood by the liver flow out of the body via the bile and digestive tract). The time of that assessment was documented at 1915 hours on May 23, 2000.

The clinical difference between bilious and non-bilious vomiting (ie, vomiting yellow or green) is critical in distinguishing life threatening abnormalities.

When a person is vomiting bile, it is pointing towards the fact that the intestine is blocked. Intestinal obstruction is typically marked by severe abdominal pain. Unlike, other inflammatory bowel diseases, where the pain is tolerable, in this case the discomfort is torturing that may subside intermittently. Abdominal pain is typically accompanied by frequent bouts of bilious vomiting. Most importantly, the person feels constipated and there is absence of bowel movement. Intestinal obstruction, especially of the proximal small bowel, produces marked nausea and vomiting of bilious material. Distention may be lacking, but intermittent cramping abdominal pain is characteristic. The word “bilious” comes from the word cholera. The word cholera is Latin for bilious disease and has come to indicate a severe intestinal infection. Acute symptoms include bilious vomiting, diffuse abdominal pain, and bloody stool. Although stomach flu is by far the most common cause, intestinal obstruction is also the most serious and is considered a surgical emergency, and treating the patient at the earliest is a must to avert any complications.

People with bowel obstructions may repeatedly vomit yellow, or green colored bile and a history of frequent bilious vomiting in the presence of abdominal pain should have been a ‘red flag’ suggesting intestinal obstruction, which should have been treated emergently. Emergency physicians have a primary obligation to treat emergency situations such as bowel obstruction. In this case it wasn't even considered. Bilious emesis is always abnormal and indicates ileus or obstruction distal to the common bile duct. The same record documents that the patient had stated she was “very tired”, whereupon she was assisted to bed, as evidenced at N-6. She also complained of being “cold” , she had the "chills" that often accompany a fever, and so the nurses provided her with extra blankets, Periods of feeling cold often occur during common illnesses, in fact the chills can often be a sign of infection that's spread throughout the body. Trauma from an infected wound can also trigger shivering. Her very last words were that she was (at that time) “feeling a little better”.

A-26 documents a body temperature >37.0°C . According to that record the documented temperature is slightly above 37°C at approximately 37.8°C, suggesting a low-grade fever. characterized by an elevation of body temperature above the normal range of 36.5–37.5°C (98–100 °F. A fever is any body temperature elevation over 100 °F (37.8 °C). Pathogenic bacteria grow best at human body temperatures in the 37 C range. Evidence of toxoemia in the form of low grade fever (37.5-38°C) has been reported in the literature. All acanthamoeba capable of growth at or above 37°C are potential pathogens - "virulence of N. fowleri is affected by growth temperature 30 to 37°C produced more virulent amoebas".

According to the medical record at N-6 Arlene Berry was admitted to the Kirkland and District Hospital at 18:45 hours and had spent 75 minutes in the ER, as evidenced at A-3. In all that time, the ED physician, Dr. Spiller had obviously done very little, as evidenced by the admission record, containing very little information.

What I take to be the physician’s diagnostic chart evidenced at A-3 of the record, is a “total blank”, like the physician whose name appears on it. Again, from that record it seems clear that nothing was entered because nothing was done. The same record was filed “out-of-sequence”. The emergency record at A-4 was also filed out-of-sequence. Interestingly both of these records were dated using a “rubber stamp” that is consistent with backdating techniques used primarily by unscrupulous healthcare providers, ie., those who have something to hide

NO simple blood tests were done or even ordered at the time of the patient's admission. TIME It is also clear that no course of action was charted, marked by a “routine” admission and a clinically evident inability on the part of the ED physician to adequately make a proper evaluation or to even make an appropriate or provisional diagnosis. Not diagnosing a condition is one of the most common forms of medical negligence. Another is when they “dismiss” the presenting symptoms as temporary, minor, or otherwise not worthy of treatment. This situation may result in an exacerbation of the underlying condition or injury, causing further harm or even death.

The record at N-6 documents “telephone orders” received by the hospital from Dr. Jordan at 2030 hours for Stemetil 10mg by IV, x 4 daily for “control of nausea”, given by the RN, as further evidenced by the physician’s orders seen at A-11 of the record. Stemetil is a brand name for prochlorperazine. Under normal circumstances, a typical single dose of Stemetil for a small woman with low body weight is 5mg.

Not only did the patient’s family physician fail to attend, but NO diagnosis or differential was made following the patient’s admission at that time, or at all, according to the record. Certainly, NO protocols were followed. A useful maxim to remember is “Not documented means not done”. Clearly, from the record as a whole, this patient was deliberately made to deteriorate w/o a diagnosis of her stomach pain.

Stemetil suppresses activity in the trigger zones of the vomiting center by “paralyzing the gastrointestinal tract” which governs the vomiting reflex, which can also exacerbate dismotility. Further, the antiemetic action of Stemetil may “mask the signs and symptoms of drug overdosage from other drugs and may obscure the diagnosis and treatment of other conditions” Increased sedation is also a serious side effect of this type of agent.

Stemetil is widely distributed into body tissues and fluids. It undergoes metabolism in the gastric mucosa and on first pass through the liver where it enters the enterohepatic circulation and is excreted chiefly in the feces via the biliary tract. The drug falls in the same class of phenothiazines that have been known to suppress intestinal motility to the point of producing a paralytic ileus and precipitate or aggravate toxic megacolon, to add insult to injury. Stemetil can also lead to changes in the blood-brain barrier (BBB), allowing an infectious agent to gain entry to the brain and produce lethal CNS ( central nervous system = brain and spinal cord) infection.

The scientific literature describe two bacterial factors specific to the meningitis pathogen that thwart the normal protective role of the blood-brain barrier, leading to serious infection. Further, parasite factors and immune-mediated mechanisms involved in blood–brain barrier dysfunction leading to neuropathogenesis have also been described. Infection of the central nervous system (CNS) can be viral, bacterial, fungal, or parasitic in origin. Blood borne infection in the blood lyse easily.

The CNS is the primary site of parasite infection for some parasitic organisms and for others, neurological infection occurs only in immunocompromised hosts. Primary amebic meningoencephalitis (PAM) and granulomatous amebic meningoencephalitis are central nervous system infections caused by free-living amebae.

http://path.upmc.edu/cases/case334/dx.html

http://path.upmc.edu/cases/case402/dx.html

It is also clear that Dr. Jordan sought to eliminate the symptom “nausea”, without his attendance, as evidenced by the phone order “for control of nausea” and without any appropriate or timely blood-work, and without addressing any possible underlying causes. For the record, know that Stemetil poisoning is marked by oversedation, respiratory depression and hypotension.

Hypotension = low blood pressure

LOW Blood Pressure Symptoms - Weak, Tired, Dizzy, Fainting, Coma

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. Stemetil (prochlorperazine) intoxication or poisoning can also cause deep physiologic depression that resembles and can mimic brain death.

Furthermore, Dr. Jordan neglected to consider bilious vomiting as a condition requiring prompt medical intervention. Instead, he elected to give the patient a brain damaging antipsychotic-antiemetic drug without any review of her medical record, and without the benefit of diagnosis, toxicological screening or close monitoring, evidenced at A-21. Clearly, the etiology of the nausea and vomiting had never been considered, apart from Dr. Spiller”s assumptive “a question has arisen” with respect to lung CA, as evidenced at A-3. Premature closure is the failure to consider other plausible diagnoses after an initial working diagnosis is reached. It is one of the most common clinical reasoning errors made by clinicians.

Monitoring should have began with a thorough history of the patient's bowel habits before starting a mega-dose of morphine combined with prochlorperazine, exascerbating the patients condition, resulting in catastrophic decline.

According to the record at A-13, Arlene Berry was given 30 mg (po bid) MS Contin (morphine) by Nurse McCrank at 2000 hours on May 23rd, the eveening before her death, in the face of an undiagnosed and undifferentiated condition(s) associated with “severe abdominal pain”. The administration of 30 mg morphine can only serve to obscure the diagnosis or clinical course in patients with acute abdominal conditions.. Morphine and prochlorperazine have a profound impact on bowel motility, often resulting in fecal impaction. The average adult carries about 15 pounds of dried fecal matter in the colon.

The co-administration of a narcotic analgesic (morphine) and a neuroleptic agent (stemetil/prochlorperazine) will result in neurolept-analgesia with drug-induced reduction of oxygen intake, resulting in respiratory depression, which represents the principal negative variable introduced with “conscious sedation” that left unrecognized and untreated, is the cause of “panic”, including most serious complications. Neurolept-analgesia, also called “conscious sedation” refers to the use of major tranquilizers, ie, prochlorperazine in conjunction with narcotics such as “morphine”. Neurolept-analgesia is defined as a state of CNS depression.

Notably, this patient had also been given penicillin-based medicines and sulfonamides such as Septra DS (Bactrim), and CIPRO (cyproflaxin) on the days before her final admission; penicillin and sulfa-based antibiotics can cause the body’s immune system to react by over stimulation. Septra DS is an antibacterial agent with a wide spectrum of adversities (difficulty breathing; closing of the throat; swelling of the lips; and unusual bleeding).

The record at A-12, what I take to be physician orders documents a concomitant or concurrent administration of MS Contin (narcotic analgesic), Statex (morphine family), and Gravol (an anticholingeric agent), including IV solution and additives, the most dangerous of which is the MS Contin, a brand name for Morphine Sulfate. “Contin”, is a pharmaceutical industry buzzword for “time-release” or “continuous” release. MS Contin has widespread effects in the central nervous system and on smooth muscle and produces respiratory depression by direct action on brainstem respiratory centers. Co-administration of narcotic analgesics such as MS Contin with laxities may have additive central nervous system (CNS) and gastrointestinal (GI) system effects which can increase the risk of severe constipation or paralytic ileus, including CNS depression. Monitoring should have began with a thorough history of the patient's bowel habits before starting these drugs.

According to the same record at A-12, Arlene Berry was given more than IV and Gravol. If not Dr. Spiller, then who ordered the 30 mg MS Contin on his watch? From that record it seems clear that either Dr. Spiller lied, or he was totally oblivious to the administration of Morphine Sulfate evidenced at A-12.

Notably, morphine is also contraindicated to sedation, or increased pressure in the head or spinal cord, possible abdominal problems requiring emergency surgery, and in patients having a substantially decreased respiratory reserve. Patients with only one lung have a decreased respiratory reserve due to diminished lung capacity. Futhermore, narcotic analgesic drugs can produce, via inhibition of peristalsis, fluid retention within the bowel great enough to mask depletion of extracellular fluid and electrolytes. CAVEAT: MS Contin overdosage may result in apnea, circulatory collapse, cardiac arrest, and breathing problems that can lead to death.

Additionally, Arlene Berry had been prescribed Statex 10 mg, another narcotic: opioid agonist analgesic which also belongs to a class of the morphine family. Statex (Morphine Sulfate) is indicated for the symptomatic relief of severe chronic pain. At no time had her Rx 10 mg dose ever been increased gradually to allow for the development of tolerance to adverse effects, for example, respiratory depression.

N-5 of the Nurses’ Notes documents “Sudden large queery bloody emesis, reddish brown liquid” at 0255 hours, on May 24th of 2000. Submit, when everything in the intestine slows down, everything in it usually backs up. When the bowel is completely obstructed, the contents back up like in a kinked garden hose. This causes the tissue to become dilated with fluid and can impair the blood supply to the intestine, causing ischemia, or tissue death. Over time, the bowel then perforates, or ruptures, causing the spillage of harmful bowel contents (semi liquid) into the abdomen. When the bowel wall is ruptured, this unsterile material contaminates the abdomen and the organs with which it comes into contact. This is extremely dangerous to a patient, as it quickly causes an inflammatory reaction called peritonitis and can lead to a system-wide infection called sepsis; indeed NO septic workup and No attempt to identify the source was ever done.

N-3 documents a “Suctioned orally thick brownish secretions” at 0320 hours (in the small hours of the morning), suggestive of a more significant backup of intestinal material, ie., vomiting of semi liquid fecal matter due to obstruction of the bowel, evidenced by family as a large brown colored (gross appearance) pasty material, looking pretty much like feces. The severe infection caused by this overflow of fecal matter can prove fatal when not treated immediately. Vomiting of fecal material (due to obstruction): If you are unable to open your bowels due to an obstruction somewhere, then your feces cannot exit your body via the normal route and you can get nauseated and start to vomit fecal matter. This condition requires urgent medical attention and probably surgery. The same record documents “suctioned down ET tube several times for small amount of brownish mucous” (a reddish brown liquid, suggestive of old blood or admixture of blood and gastric content) at 0330 hours, while A-17 documents “being suctioned for moderate amounts of coffee-ground emesis by RN” at the very same time.

Suctioning infers that the patient’s airway has become obstructed with secretions or debris. When an individual has an infection or illness, it creates the conditions allowing mucus to accumulate in the throat. Any negligence of the patient’s throat secretions may lead to hypoxia, brain edema and further deterioration in a patient’s condition leading to a vicious circle, which if not broken will lead to death.

The record at A-5 documents a blood pressure of 115/75 at 17:05 hours on May 23rd that by 18:45 hours had dropped to 100/50 bpm. Unlike high blood pressure, low blood pressure is defined primarily by signs and symptoms of low blood flow and not by a specific blood pressure number.

A-20 of the record documents a Glucose of 13.2 H mmol/L (the normal range is 4.1 – 7.8). High blood sugar usually comes on slowly. To convert mmol/l of glucose to mg/dl, multiply by 18. (13.2 x 18) = 237.6 mg/dl. Glucose is 13.2 H mmol/L = 237.6 mg/dl. Symptoms of severe high blood sugar (hyperglycemia) include drowsiness and difficulty waking up. Acute, short-term hyperglycemia may precipitate vascular occlusions by facilitating platelet activation. With infection, blood sugar levels tend to rise quickly over several hours. Certain drugs can also affect blood sugar levels. It should also be borne in mind that certain medications such as Morphine and phenothiazine derivatives such as Stemetil actually contribute to the occurance of hyperglycemia. In fact, both have been reported to trigger diabetes in patients with no previous history of diabetes. See transient hyperglycemia.

A-19 of the record documents an elevated WBC Count of 22.4 H. The presence of an elevated WBC count is called Leukocytosis. An increase in WBCs may occur in many conditions, including infection (viral, bacterial, fungal, and parasitic), allergy, leukemia, hemorrhage, traumatic tap, encephalitis, and Guillain-Barre syndrome (GBS). When the number of WBCs in your blood increases, this is a sign of an infection somewhere in your body. Prior infection is well established as a precipitating event in the development of GBS.

http://science.howstuffworks.com/life/human-biology/blood2.htm

WBC’s (leukocytes) are the body’s primary defense against infection and also reflect the degree of physiologic stress. WBC’s are also elevated with dehydration, and hyperviscosity secondary to dehydration. A high WBC may also indicate that there is inflammation of the central nervous system as in meningitis, for example. The WBC differential helps to distinguish many of these causes. For example, viral infection is usually associated with an increase in lymphocytes, while bacterial, fungal and certain parasitic infections are associated with an increase in polymorphonuclear leukocytes (neutrophils). More precisely, migration of Polymorphonuclear leukocytes (PMNL) across epithelial linings is a hallmark of several gastrointestinal (GI) disorders. Moreover, the presence of PMNL is noted in gastroenterocolitis induced by ischemic conditions, and by various toxic or drugs. PMNL transepithelial migration is also a key feature of acute phase of idiopathic inflammatory bowel diseases (IBD) (Crohn’s disease and ulcerative colitis). Moreover, the degree of PMNL infiltration in intestinal mucosa is one of the most important criteria of disease activity.

The histological hallmark of ulcerative colitis is polymorphonuclear leukocyte invasion of the mucosa and sometimes of the sub-mucosa of the colon. Ulcerative colitis is an inflammatory bowel disease that affects the lining of the large intestine, also called the colon. The disease usually causes diarrhea, blood in the stool, and abdominal pain, and can also lead to nausea, lack of appetite, weight loss, and anemia. In addition, malaise, anorexia, weight loss, moderate to severe abdominal pain, low grade fever, chills, muscle pain, signs of peritonitis, toxemia, and other systemic symptoms may be present. Incontinence is often a problem especially when the rectum is severely inflamed. Amoebic Colitis has been found to be associated with progressive abdominal pain, and signs of peritonitis, leukocytosis, hyponatremia, hypokalemia, bloody mucoid diarrhea and dehydration.

While diarrhea, pain, and blood in the feces are common with Ulcerative colitis, the extent of disease varies greatly from person to person. Severity of disease is categorized as mild, moderate, or severe according to clinical symptoms. In severe cases, patients experience frequent episodes of bloody stools and they may become anorectic and nauseated. In severe attacks, patients may vomit and experience symptoms of anemia such as breathlessness, and fatigue. Weight loss, fever, fast heartbeat, dizziness, and severe cramping or abdominal pain can also occur with severe cases of the disease. .The most common early symptoms of ulcerative colitis are constipation with passage of blood or mucus in the stools. Untreated patients may develop toxic megacolon. Potential for central nervous system toxicity. The use of opioids can lead to a rapid deterioration and colonic perforation.

The typical lesion doctors see in ulcerative colitis is called a "crypt abscess" and are located in the mucosa of the large intestine. The major organs of the abdomen include the small intestine, large intestine, and stomach. The presentation of abdominal abscess is similar to that of peritonitis, but the symptoms are generally milder.

The most feared complication from severe ulcerative colitis is toxic megacolon. . Perforations can also occur in severe ulcerative colitis even if toxic megacolon does not develop. Most perforations occur in the left colon, commonly in the sigmoid colon. Perforations tend to occur more often during first episodes of colitis. Perforations must be treated surgically.

Among the possible environmental factors, no specific foods have been identified as a cause of ulcerative colitis (UC). Possible risk factors include immunologic factors, infectious agents (such as bacteria, viruses, or amoebae), and dietary factors (including chemicals and drugs). Some people with ulcerative colitis are intolerant of cows' milk and find that dairy products may aggravate symptoms. Cigarette smoking actually reduces the risk, though what component of tobacco has a beneficial effect on the colon lining is not entirely clear. Smokers have only about 40 percent of the risk of developing ulcerative colitis of nonsmokers.

If the total WBC is high due to a rise in neutrophils and eosinophils, then an allergic, or parasitic process is most likely.  The antipsychotic and anti-nausea drug Stemetil is also known to cause neutrophilia. Other causes of an increased neutrophil count include cerebral abscess. Bleeding leads to hypotension, tachycardia and most probably sepsis. Neutrophils rush in to fight of infection.

An increase in the WBC count is also a typical response to noxious stimuli.

The record at A-19 documents a Neutrophil count of 92.0 H with an Absolute Neuts of 20.0 H. Neutrophilia (or neutrophil leukocytosis) is a condition where a person has a high number of neutrophil granulocytes in their blood. Normally, neutrophils account for 50-70% of all leukocytes. If the count exceeds this amount, the cause is usually due to an acute infection. Neutrophils, are also known as “segs”,”PMNs” or “polys”(polymorphonuclears). PMNs are the primary effector cells in the innate immune response against infection. A high neutrophil blood count is a sign that something in your body has triggered an immune response.  People with cancer, though, often have fewer neutrophils patrolling the body. In some cases that's because the cancer itself damages the bone marrow, the spongy material inside the bones where all new blood cells — including neutrophils — are made. (This is especially common with cancers like leukemia and lymphoma.)

http://www.ncbi.nlm.nih.gov/pubmed/18831680

Polymorphonuclear leukocytes (granulocytes) accumulates in brain regions with low blood flow during the early postischemic period. Polymorphonuclear cells (PMNs) usually represent the predominant cell type in an inflammatory response, acting as the first line of defence against invading organisms. Neutrophilia may also be due to a number of acute and chronic causes such as infection, inflammation, emotional stimuli, drugs, metabolic hormonal, and endocrine disturbances, including hematologic abnormalities. The ratio of neutrophil and lymphocyte counts has even higher value in predicting bacteremia. Normally, neutrophils account for 50-70% of all leukocytes. If the count exceeds this amount, the cause is usually due to an acute infection.

Leukocytosis, especially neutrophilia, indicates systemic infection and is rare in the absence of bacterial “superinfection”, also called “superbugs”, such as bacteria, viruses or mixed infections which are resistant to antibiotics. Neutrophils are also associated significantly with the density of parasites, such as seen in amebic colitis. It has been suggested that the damage observed in invasive amebiasis is related to interactions between polymorphonuclear leukocytes (PMN) and Entamoeba histolytica.

There are two basic types of leukocytes. The phagocytes are cells that chew up invading organisms and the lymphocytes are cells that allow the body to remember and recognize previous invaders. Neutrophilia facilitates the inflammatory response, whereas when neutropenia is present, the inflammatory response to such infections is ineffective. The end result is an autoimmune reaction. The immune system fails to properly distinguish between self and non-self, and attacks part of the body.

Autoimmune disorders occur if the body’s immune system mistakenly attacks the body’s cells and tissues. A low lymphocytes count (lymphocytopenia) results in the inability to remember and recognize and hence fails to distinguish.

Molecular mimicry leads to autoimmunity because the parasites activate lymphocytes that cross-react where a foreign antigen shares sequence or structural similarities with self-antigens. Molecular mimicry has typically been characterized on an antibody or T cell level. The most commonly proposed mechanism for the development of autoimmune disease is molecular mimicry (Yuki, 2005). Molecular mimicry refers to the situation where the pathogen and host share nearly identical antigens, which induces an antibody and T cell immune response that is cross reactive. Notably, the granulomas of sarcoidosis are caused by collections of immune system cells, particularly T cells. Aggressive mimicry is a form of mimicry where predators, parasites or parasitoids share similar signals with a harmless model, allowing them to avoid being correctly identified by their prey or host .

The record at A-19 documents a Lymphocyte count of 2.0 L (low), is the condition of having an abnormally low level of lymphocytes in the blood.Lymphocytopenia, or lymphopenia, can range from mild to severe. The most common causes for lymphocytopenia are autoimmune disorders.

An autoimmune disorder is a condition that occurs when the immune system mistakenly attacks and destroys healthy body tissue. There are more than 80 different types of autoimmune disorders. If someone with lymphocytopenia gets any kind of infection, it has to be treated as an emergency. Even minor problems can progress much more seriously for people with this disorder than they would for people with normal immune systems. A low lymphocyte count makes it hard for your body to fight infections.

People with lymphocytopenia have a weakened immune system and tend to get a lot of unusual infections. due to reduced antibody production (a weakened immune system is mainly caused by the presence of toxins in your body). Lymphocytes help protect your body from infection. Lymphocytopenia has a wide range of possible causes. A low lymphocytes count (lymphocytopenia) results in the inability to remember and recognize and hence fails to distinguish. A low lymphocyte count indicates that the body's resistance to fight infection is substantially reduced. Neurological as well as autoimmune diseases too can decrease lymphocytes in the body.

People who have too few T lymphocytes or too few natural killer cells have problems controlling certain infections, especially viral, fungal, and parasitic infections. Absolute lymphocytopenia is a predictor of bacteremia. Severe lymphocyte deficiencies can result in uncontrolled infections that can be fatal. Absolute lymphocytopenia can also be used in the prediction of infectious emergency admissions. Lymphs is an abbreviation for lymphocytes. These white blood cells are also responsible for fighting infection and also develop antibodies to protect the body against future attacks. Low levels can indicate viral infections affecting the bone marrow or sepsis. Lymphocytopenia can also be a side effect of radiation treatment.

Your low lymphocytes are what we expect to see in sarcoidosis. Th1 diseases are lymphopenic, which means a lack of T-cells. This is because the T-cells play only a minor role in Th1 disease. The bacteria inside the phagocytes directly activate the phagocytes, there is no need for any T-cell recognition of pathogens, and so the body down-regulates the number of T-cells it manufactures (hence the lymphopenia).

Idiopathic CD4 lymphocytopenia (ICL) is a presumed heterogenous syndrome with key element low CD4 T-cell counts (below 300/mm3) without evidence of HIV infection or other known immunodeficiency. The clinical presentation can range from serious opportunistic infections to incidentally diagnosed asymptomatic individuals.

Amebiasis (amebic dysentery) . It is an asymptomatic carrier state in most individuals, but diseases ranging from chronic, mild diarrhea to fulminant dysentery may occur. Infection with the amoeba Entamoeba histolytica can cause amoebic dysentery. Severe amoebiasis infections (known as invasive or fulminant amoebiasis) occur in two major forms. Invasion of the intestinal lining causes amoebic dysentery or amoebic colitis. If the parasite reaches the bloodstream it can spread through the body.

Sarcoidosis and opportunistic infections? Opportunistic infections can resemble sarcoidosis. They can also co-exist with sarcoidosis. Granulomatous reaction consistent with sarcoidosis?

SEARCH: Mixed connective tissue disease and overlap syndromes. Brain abscess are usually mixed infection. Some diseases are caused by the infection by more than one type of organism simultaneously.

A-19 documents an RBC (red blood cell) count of 4.30 (3.80 – 5.80 is normal), but the HCT (hematocrit) is very low, with a reduction suggestive of anemia (a blood condition in which there is a decreased amount of oxygen-carrying hemoglobin in the blood and, usually, fewer than normal numbers of red blood cells), or a decrease in the number of red blood cells caused by anemias or blood loss. SIgns of increasing anemia include pallor, lethargy, irritability, and poor appetite.

A-19 documents a hemoglobin of 120 (120-160 is normal). - measures the amount of the oxygen-carrying protein in the blood. If the RBC and the hemoglobin are both normal, it is possible to estimate the hematocrit as being approximately three times the hemoglobin. The same record documents an HCT (Hematocrit) count of only 0.361 L (low). HCT is a measurement of the fractional volume of red blood cells. This is a key indicator of the body’s state of hydration, anemia or severe blood loss, as well as the blood’s ability to transport oxygen. A decreased hematocrit can be due to either overhydration, which increases the plasma volume, or a decrease in the number of red blood cells caused by anemias or blood loss. The loss of blood can cause iron deficiency, anemia and dizziness.

A hematocrit test is frequently done to assess the extent of significant blood loss. If a person with a normal blood cell volume loses blood suddenly through a massive hemorrhage, the person may develop signs and symptoms of circulatory shock; the blood pressure will fall and the patient will show signs of tissue hypoxia and shock.

HCT is also the measurement of the percentage of red blood cells (RBC’s) in whole blood and in this case it is very low. Thus anemia is present when HCT is < 1.0 x 109/L. The result is a lot fewer red blood cells to carry oxygen. The patient is usually noticeably pale.

Parasite infection may provoke significant reduction in hematocrit, mean corpuscular volume, mean corpuscular haemoglobin concentration and lymphocyte percentage.

A-19 also documents a Monocyte count is 3.0, 2.0 – 10.0. The monocytes are a type of phagocyte which mature into “macrophages”; they are also important germ eating cells. Patients with a low monocyte count have a higher risk of getting sick from an infection. In this case, the Monocyte count is in the low normal range.

In cancer, or leukemia, the monocytes usually become elevated; cancers tend to raise blood monocyte levels. Malignant conditions such as leukemia or lung cancer can lead to increased monocyte levels, along with raised levels of other types of white blood cells.

A-19 further documents an RDW of 18.4 H. Red cell distribution width (abbreviated as RDW) is a measurement of the amount that red blood cells vary in size. Red blood cells help carry oxygen in the blood An elevated RDW (red blood cells of unequal sizes) is known as anisocytosis . Anisocytosis is a medical term meaning that a patient's red blood cells are of unequal size. This is commonly found in anemia and other blood conditions. The normal RDW level is 11.5-16.8.

A-20 documents the O2 Sat (oxygen saturation) with an arterial oxygen saturation (SaO2) of 98.9 H . (95-98 is normal). The oxygen saturation is the amount of oxygen actually carried by the hemoglobin. Normal oxygen saturation values are 97% to 99% in the healthy individual.Arterial blood gas determinations will indicate two basic bodily functions:

1. acid-base balance of the blood
2.oxygenation status of the blood.

http://www.rnceus.com/abgs/abgoxygen.html

An arterial PO2 (Partial Pressure of Oxygen) of 129.0 H (75-100 is normal). If high, patient may be over ventilated.

A-20 documents a pO2 of 129.0 H. The PO2 measures the amount of dissolved oxygen in the blood and is measured in mmHg. The normal reference range is 78-100 mmHg. High oxygen concentrations predispose to oxygen toxicity. The first and most important method to prevent pulmonary oxygen toxicity is to limit exposure to the lowest possible pO2.

Elevated pO2 levels are associated with:

Increased oxygen levels in the inhaled air

Polycythemia

A-20 documents an Arterial pH of 7.437. A normal pH is 7.35 – 7.45. The ideal pH for blood is 7.4. With a blood pH of 7.437 the pH is optimal. The time of that assessment is documented at 0400 hours on May 24th of 2000. Notably, the kidney and the liver are two main organs responsible for the metabolic homeostasis of pH. The same record documenst a Base Excess of 1.0 with a reference range of 2.0. If the base excess is less than – 2, then there is a metabolic acidosis, which may be the compensatory process.

Be aware that patients can have mixed metabolic disorders (eg. concurrent metabolic acidosis and alkalosis) that can give them a pH in the normal range.

Hydrogen ion concentration expressed as pH “Power of Hydrogen” (Humans as organisms) scale of acidity/alkalinity. pH below 7 = acidic, pH above 7 = alkaline. Neutral pH is 7, in this case on the alkalemic side of normal. Acids and alkalis are the chemicals at each end of the pH spectrum. The scale runs from 0 (acid) to 14 (alkali). For example, the pH of blood is normally 7.4 and that of muscle is 7.0. pH under 7 is acid; pH over 7 is basic or alkaline. The metabolic pathways of the body require a slightly alkaline environment. Ph 7.0 and higher indicates alkalinity.

Our blood pH has a very narrow range of around 7.35 to 7.45. If our body’s pH deviates from this range, we will be sick or have symptoms of falling sick. a blood with a pH value of 7.45 contains 64.9% more oxygen than blood with a pH value of 7.30. The heart is normal when the pH of blood plasma is slightly alkaline, having a pH of 7.35 to 7.41. An absolute blood measurement of acidity (pH below 7.0) is incompatible with sustaining life.

It is a known fact that cancer thrives in an acidic (pH) environment in the body, but cannot survive in an alkaline (pH) environment. At a pH slightly > 7.4 cancer cells become dormant. With metastases the pH drops to 6.0 and even 5.7 or lower. Terminal cancer patients are around 1000 times more acidic than normal healthy people. The vast majority of terminal cancer patients possess a very low body pH. In the case of Arlene Berry, her pH was optimal - as good as it gets. With a diagnosis of metastic cancer, someone is trying to pull a fast one here.

A-18 of the medical record documents a possible “inferior ischemia”, a sign of reduced oxygen supply to vital organs due to reduced or poor blood flow to the heart. Inferior ischemia means that a portion of your heart (lower) muscle is not getting enough blood supply. It usually occurs as a result of a blockage in one of the arteries supplying that portion of the heart muscle with oxygen.

Inferior ischemia is decreased blood flow to part of the heart (the inferior part). This is a serious condition, and can be predictive of what is commonly known as a “heart attack”. An inferior ischemia is the hallmark of “impaired organ perfusion”, as it implies that, unless corrected, there may not be enough oxygen in the blood to sustain vital organs; inadequate cerebral perfusion can be avoided by removing vasoconstricting factor(s), improving peripheral blood flow, reducing metabolic demands on the body.

The same record at A-18 documents “Sinus Tachycardia”. It occurs when the sinus rhythm is faster than 100 beats per minute (bpm) ; also associated with shock, hypotension, hypoxia, congestive heart failure, and various high output states. Most often sinus tachycardia is caused by an increase in the body's demand for oxygen; sinus tachycardia can have serious consequences and put the patient at risk for iatrogenic harm, ie right bundle branch block (RBBB). The right bundle branch receives most of its blood supply from septal branches of the left anterior descending coronary artery, particularly in its initial course.

http://www.uptodate.com/contents/sinus-tachycardia

A-20 documents a CK (Creatine Kinase) level of only 40 units per liter (U/L) at 0400 hours. In females, total Creatine Kinase should be 10-79 units per liter (U/L). The creatine kinase level usually parallels a disease activity. In normal conditions, there is very little Creatine Kinase circulating in the blood of the average, healthy human being. Know that 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.

The hallmark of muscle wasting (or muscle damage) is elevation of CK. The wasting away of fat and muscle (cachexia), is the most visible hallmark of metastatic cancer. Persons with cancer typically have high CK levels. Elevation of CK may also be seen in stroke, extreme shock, and brain tumors in which CK levels can sometimes temporarily go off the scale, topping out at 50,000 to 200,000 U/L, a sign of severe muscle fiber breakdown (necrosis). CK levels may rise significantly in about 2 to 3 hours. Taking a good history is important in these circumstances.

Significant increases in serum CK have been observed and reported in cases of adenocarcinoma and SCAC of the lung with proven CNS metastases, while patients with oncological conditions other than SCAC of the lung have failed to show elevation in serum CK. Also, in various cases of infectious myositis, muscle enzymes such as creatine kinase are paradoxically normal despite muscle inflammation. In this case, CK is well within the normal range. Serum CK is considered a useful diagnostic marker or indicator of active metastases.

A normal Creatine Kinase (CK) at the time of the patient's admission to hospital on May 23rd of 2000, would argue favorably against a diagnosis of metastatic CA.

A-20 of the record also documents a Serum Potassium level of 3.4 L at 0400 hours on May 24th of 2000. Hypokalemia is defined as a potassium level below 3.5 mEq/L. Hypokalemia is a metabolic disorder that occurs when the level of potassium in the blood drops too low. The two major causes for the loss of potassium from the digestive system can be vomiting and diarrhea. In addition to common symptoms such as vomiting, nausea, constipations, hypotension and a list of at least 22 different symptoms, muscle weakness is the most predominant.

Hypokalemia may also cause slow movement of the colon.

N-10 of the Nurses’ Notes document the patient’s level of care as “routine”, which shows little or NO concern for patient safety. Further, NO close patient monitoring or toxicological screening was ever done or even suggested, marked by a complete absence of nursing care plan, as evidenced at A-21 of the record. In fact, NO bloodwork was done in a timely manner. NO protocols were ever implemented, in this case.

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”, usually the result of proprioception, or loss of sense of one’s own perception of the relative position of neighboring parts of the body to each other, which is occasionally impaired spontaneously, especially with extreme fatigue. In the alternative, could this have been the result of a transient ischaemic attack (TIA), possibly due to inappropriate treatment, or perhaps as a presenting clinical manifestation of an undiagnosed condition, such as sarcoidosis ? In a transient ischaemic attack (TIA),your brain is temporarily starved of oxygen and nutrients by having the blood supply blocked. A TIA (Mini-Stroke) happens suddenly, without warning. The blood flow may be reduced by a narrowing or blockage of the blood vessels, or granulomas clustered around blood vessels.

The ED physician, Dr. Spiller was up to assess the patient’s condition. Upon examination her eyes were documented as being “sluggish”. Her “pupils were dilated at approx. 5 mm” with “very little reaction to light”, and far from getting better she was becoming progressively worse, as evidenced by a sense of urgency seen on the record to the attendance of the patient with increased activity evidenced at N-6 between 0030 and 0055 hours, also noted at N-5. The same record documents “no response to verbal or physical stimulation, repositioned by nurses in bed & placed right lateral position”. The position of the body during sleep can have a significant effect on the development of Cheyne-Stokes breathing. Data seems to suggest that sleeping supine and at a flat head angle can significantly increase the likelihood of Cheyne-Stokes breathing.

Clearly, from the record and apart from running around the room looking busy and repositioning the patient, nothing was done. It seems clear that the ED physician failed to properly assess the patient’s condition, which fell far below an acceptable standard of care. Further, to add insult to injury, NO blood-work had yet been done.

While the clinical feature of 'dilated pupils’ is a valuable clinical sign - it can occur with a number of conditions.

I assume that Dr. Jordan would have been alerted by phone. He claims to have called in at 0100 hours but nevertheless opted not to change his orders, as evidenced by the “no change in orders” seen at N-5. From that record it is clear that Dr. Jordan elected to alienate the patient and treat her over the telephone, unseen, in the face of life threatening indicators, all of them ignored and without ever having reviewed the patient record.

Further, between 0200 hours and 0220 hours the patient’s blood pressure had risen slightly from 150/72 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 assessment as 0220 hours, while N-5 documents the time of the same assessment at 0230 hours, a 10 minute difference. The same record documents a HR (heart rate) in the 160's, what is termed “sinus tachycardia”, being defined as a sinus rhythm with a rate exceeding 100 bpm, often the result of a panic attack.

A-26 documents a blood pressure of 162/80 with an SaO2 of only 80% at 0220 hours, followed by a potentially lethal drop in blood pressure to 78/70 by 0235 hours.

CAVEAT: Systolic blood pressure < 80 mm HG is a hallmark of haemodynamic instability. The term “hemodynamic instability” is most commonly associated with an abnormal or unstable blood pressure, especially hypotension, or trauma due to clinical insult. Hemodynamic instability has also been defined more broadly as global or regional perfusion that is not adequate to support normal organ function.

The record at A-17 documents a complete cessation of the use of abdominal and accessory muscles, evidenced by a “0 use of acc muscles”; and a “0 use of abd muscles”; the muscles of respiration, accessory muscles and diaphragm are affected, suggestive of respiratory and accessory muscle paralysis (crisis) requiring intubation and mechanical ventilation. The time of that assessement is documented at 0330 hours. Accessory muscle paralysis will result in apprehension and anxiety. = panic.

A-24 of the record documents a heart rate of 174 beats per minute (bpm) at 0320 hours that is consistent with Ventricular Tachycardia (VT). With ventricular tachycardia the rate is in the range of 170 beats per minute or more; a cardiac arrhythmia in which the muscles of the ventricles contract irregularly in a rapid, uncoordinated manner, impairing the normal pumping of blood, and is recognized as one of the shockable rhythms on the cardiac arrest protocol. A normal resting heart rate for adults ranges from 60 to 100 beats a minute. Ventricular tachycardia (VT or V-tach) is a potentially life-threatening cardiac arrhythmia that originates in the ventricles. It is usually a regular, wide complex tachycardia with a rate between 120 and 250 beats per minute. Ventricular tachycardia has the potential of degrading to the more serious ventricular fibrillation. VT can occur with or without heart disease.

Ventricular tachycardia is a common, and often lethal, complication of a myocardial infarction (heart attack). An episode of extreme terror (pain fright, extreme emotional stress), can also result in ventricular tachycardia, and potentially culminate in death.

A viral or bacterial infection of the heart muscle (myocarditis) High blood pressure (hypertension) A blood clot in the lungs (pulmonary embolism)

EVIDENCE OF ALTERED RECORDS

There are numerous material deficiencies in the related medical record of Arlene Berry which manifest a complete lack of internal consistency, ranging from out of sequence records, from the physician’s discharge note seen at A-1 and A-2, to the nurses Triage, to obviously rewritten, altered, and/or falsified medical records seen between N-1 and N-3 of the Nurses Notes, which are marred by error, inconsistency, omission, and contradiction, with A-16, and A-17 presenting similarly. The records were unsequentially numbered from back to front, and dubiously tailored to obscure and obfuscate the truth.

A-26 of the record documents a BP (blood pressure) of 78/70 at 0235 hours, while the record at N-5 documents a BP of 98/70 at the very same time, suggestive of "scribe errors". Question is, who copied who, and/or who altered what? The answer is quite simple in that whatever answer tends to 'lessen or mitigate' the circumstance, wrongdoing, or outcome of an event, being the wrong answer, in the presence of two or more conflicting entries invaribly points to the truth. The correct answer is therefore a BP of 78/70 mm Hg, being a truly narrow pulse pressure. Low blood pressure , also called hypotension, is blood pressure that is low enough that the flow of blood to the organs of the body is inadequate.

Profound hypotension with reduced tissue perfusion?
Low blood pressure, or hypotension, occurs when blood pressure during and after each heartbeat is much lower than usual. This means the heart, brain, and other parts of the body do not get enough blood.

A-4 of the record, what I take to be a Trauma record, barely visible in the physician’s notes situated in the lower right hand side of that record, there is an obliterated area suggesting a white-out, or perhaps an erasure. From that record it seems clear that relevant information may have been deliberately removed to conceal a traumatic event. TRAUMA is defined as any insult to the body, clinical or otherwise.

The record at A-6 documents a “history of metastatic lung cancer”, while the outpatient record at OP-54 clearly documents “no metastasis” and “mediastinoscopy negative”.

Hematologic results included neutrophilic leukocytosis and lymphopenia.

RadiationTherapy probably caused immunosuppression and increased susceptibility to infection. Alternatively, this is often caused by medications that suppress the immune system.

Notably, a presumptive diagnosis of bronchitis was made.

Most lung cancers are not visualized with the bronchoscope because they are located toward the edge of the lung, rather than in a major bronchus. A false positive test can occur in the presence of inflammation or infection.

Sarcoidosis is an inflammation in which lymphocytes become overactive. These overactive lymphocytes release chemical substances which cause granulomas (a collection of inflammatory cells) in various organs of the body. Although sarcoidosis is a multisystem disorder, it affects the lungs 90% of the time, making it primarily a lung disease.

The most common symptoms of a parasite infection include constipation, diarrhea, gas and bloating, irritable bowel syndrome, joint and muscle aches, anemia, allergies, skin conditions, tumors, nervousness, sleep disorders, teeth grinding, chronic fatigue, and immune dysfunction. Severe parasitic infections in the bile duct or the intestines can make bowel movements difficult, leading to worsened symptoms of constipation.

However, intestinal invasive amoebiasis may be associated with a variety of anatomical alterations such as acute ulcerative colitis, toxic megacolon, ameboma, or amebic appendicitis.

Parasites are the most undiagnosed condition in Canada and the U.S. The symptoms they cause are many and varied. In this case, could the symptoms have been missed due to insufficient clinical investigation of the work-relatedness of patient symptoms?


physician assigned codes

ICD-9-CM Diagnosis Code 599.0 Urinary tract infection
784.0 : Headache
787.03 : Vomiting
599.7 Hematuria

N-4 presents with less than half a page of documentation consistent with deliberate omission, such as having rewritten that record for the express purpose of withholding incriminating information.

A-16 documents a blood pressure of 163/117 at 0330 hours while N-3 documents a blood pressure of 136/85 at the very same time. The same record documents a blood pressure of 121/81 at 0400 hours, while N-2 documents a blood pressure of 112/57 at the very same time.

NORMAL Blood Pressure is 120/80.

N-4 of the record documents that Dr. Jordan was called in at 0225 hours. A-1 of the record documents “I was called in later that night because the patient had become obtunded.”

N-2 documents “attempts to pull away to painful stimuli” as late as 0400 hours on May 24th, suggests a state of stupor marked by mental dullness. one hour and thirty-five minutes after Dr. Jordan was called in,

Stupor is an excessively long or deep sleeplike state. A person can be aroused from it only briefly by vigorous stimulation, such as repeated shaking, loud calling, pinching, or sticking with a pin. Reactions to certain drugs, dehydration, and infections are common causes of impaired consciousness. In coma, a person is highly unlikely be roused to painful stimulation.

Was it the doctor’s belief that Arlene Berry ceased to be a human being after becoming unresponsive following undiagnosed, untreated and/or inappropriately treated conditions? So much so that he decided to write her off? Or was there a more sinister plot afoot? He showed absolutely no concern for her wellbeing.

N-10 of the record with respect to the patient’s bowel routine for toileting is a complete blank, with the very same information that ought to have been recorded, also omitted at OP-53 of the record. Notably, OP-51 and OP-52 of the record were withheld altogether.

The record at N-5 documents a physician “assessments unchanged” at 0235 hours despite the fact that the patient had already gone into respiratory distress at that time, 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. includjng pulmonary dysfunction. It occurs when something obstructs breathing in the upper airway. People with sleep apnea stop and restart breathing multiple times while sleeping. Snoring and gasping for breath are part of the same problem. Cheyne–Stokes respiration is mainly seen in severe heart failure, but it may also occur in normal persons during sleep. Neurologic causes include stroke, tumours, meningitis, encephalitis, and trauma. Obstructive sleep apnea occurs when the muscles in the back of your throat relax – likely drug-induced (such as due to opiate toxicity).

Drugs, such as opioids (narcotics), may cause diffuse brain dysfunction if people are sensitive to their effects or if the level of drug in the blood is too high. Other causes include panic attacks.

Low oxygen saturation may be present with advanced respiratory muscle involvement. If proper balance is not promptly restored or corrected, the heart and lungs may fail and the brain will literally begin to suffocate.

The record at N-5 documents the respirations as “deep and soaring without constant jaw lift”as early as 0220 hours, and is often a side-effect of morphine administration. Morphine distributes to skeletal muscle, kidneys, liver, intestinal tract, lungs, spleen, and brain.

http://www.breathsounds.org/docs/Breathing%20Patterns.pdf

A-26 of the record documents “gurgling” sounds , suggestive of elimination changes, as evidenced in the lower left corner of that record. Abdominal rumblings and gurglings (a gurgling or growling stomach) are particularly associated with parasitic invasion. Parasitic invasion is often mistaken for vague digestive problems, including flu-like symptoms, colitis, stomach aches, nausea, unexplained vomiting, etc.

N-5 of the record documents “family in” at 0250 hours. On seeing the patient, we found her to be propped up in the arms of two nurses, gasping for air, with only a plastic oral airway in her mouth. A reason for this , according to the duty nurse was “to keep the patient from swallowing her tongue”. Weakness of tongue and retropharyngeal muscles causes positional airway obstruction which can occur in unconscious supine patients; difficulty with protruding tongue and difficulty swallowing indicate that bulbar involvement is significant. Motor neuropathy with conduction block.

Loss of gag reflex, airway compromise - respiratory compromise is likely due to airway obstruction.Noise heard during any part of the respiratory cycle may indicate airway obstruction or alteration in airway patency. Noisy breathing suggests airway compromise.

Patients with neuromuscular disorders have rapid, shallow breathing secondary to severe muscle weakness, which requires that these patients be placed on ventilators in order to breathe. Failure to manage the airway with endotracheal intubation when necessary or in a timely manner is clear evidence of negligence.

I had asked the patient twice, in the presence of her foster brother, if she could hear me to wiggle her toes, and indeed she did, not once but twice, to be absolutely certain. An observation made by her foster brother as he gently stroked her right cheek was the seeming appearance of the patient attempting to pull her face forward as though trying to lift her head off the pillow. She had been placed in a supine position. The inability to lift the head off the pillow by flexing the neck is danger sign that frequently develops simultaneously with phrenic nerve (diaphram) weakness, such as seen in thoracic outlet obstruction, or peripheral neuropathy. This disorder is primarily recorded in persons with diabetes, compromised immune systems, or those who have suffered some sort of injury to these nerves.

Peripheral neuropathy is damage to nerves of the peripheral nervous system, which may be caused either by diseases of or trauma to the nerve or the side effects of systemic illness. Compare –Toxic, metabolic, infectious, inflammatory.

In my opinion, Arlene Berry appeared to be more paralyzed or blunted than anything, with the exception of lower limb joint contractions which rapidly diminished.

Her condition on the night before her death was cataleptic-like, characterized by a profound hypnotic state, or psychomotor condition of morbid sleep, such as seen in those who have experienced significant stress, severe emotional trauma, emotional shock, serious infection, immune-system dysfunction, or exposure to toxins, Compare: neuroleptanalgesia (conscious sedation) in combination with a severely paralyzed motor function.

Although patients with GBS in the setting of preserved consciousness may appear to be completely obtunded, they are technically awake and fully lucid. But he/she may literally not be able to move a muscle in response. The GBS  patient only appears to be unresponsive due to a severely paralyzed motor function. It has been shown that more than half of the time it is the family and not the physician who first realized that the patient was aware.
Stupor and coma are characterized by impairment of the arousal system. In stupor, a person arouses only in response to strong verbalor tactile stimuli, awakens briefly, and then lapses back into a sleep-like state after the stimulation stops. In coma, a person cannot be roused to consciousness.

N-3 of the record documents “resp noisy”,”shallow”, “Cheyne-stoke” at 0320 hours. Cheyne-stokes breathing is a respiratory pattern that oscillates between hypoventilation and hyperventilation, usually the result of diencephalic insult. It may also be seen during sleep in some normal individuals.

Hyperventilation = too much gas exchange. Hypoventilation = not enough gas exchange.

N-5 documents a “sudden large bloody-emesis of reddish brown” at 0255 hours , what is known in medical circles as “coffee-ground emesis” ie. dark brown tinged vomit the color and consistency of coffee-grounds, composed of gastric juices and old blood, which can rapidly grow bacteria.

Vomit that contains blood may have a red or brownish red appearance and is called coffee ground emesis, indicating that it has come from large intestines, suggestive of a slow bleeding source in the upper GI tract. Obstruction below the middle of the small bowel also gives rise to brownish vomit.

Gastrointestinal (GI) bleeding due to stress ulceration in GBS is reported in the literature. GI bleeding is considered a potential medical emergency. It involves assessing hemodynamic stability, resuscitating the patient as needed, locating the source of the bleed, and treating the underlying cause.

From the record it seems clean that NO emergency measures were taken with respect to GI bleeding and that this medical EMERGENCY event was met by the doctors with complete indifference.

The record at N-4 documents “incontinent blood tinged urine”at 0305 hours. Incontinent “tinged urine” is consistent with dehydration, often mistaken for hematuria (blood in urine). Incontinence can also be the result of hypotonia, or neurogenic bladder. Urinary incontinence can be a symptom of both over-hydration and dehydration. Hematuria is inconsistent with a “large amount of dilute urine” documented at N-3 of the record, suggestive of dehydration;

abnormal urine color can be mistaken for blood and decreased or absent urine output (oliguria) inadequate fluid intake.

Notably, N-3 of the record documents a “large amount of dilute urine” (polyuria) at 0325 hours, only 20 minutes later. This finding is inconsistent with hematuria, but may suggest diabetes insipidus, or a patient demonstrated hypotonic hyponatremia with maximally dilute urine consistent with IV overload.

Because of the excretion of abnormally large volumes of dilute urine, you may quickly become dehydrated.

The color and volume of urine can be reliable indicators of hydration level. The output of a large volume of dilute urine leads to extracellular dehydration.

A common cause of hyponatraemia is hypotonic dehydration and iatrogenic water overload (eg overestimation of the degree of dehydration, inappropriate use of hypotonic solutions for rehydration and/or too rapid administration of maintenance fluids). Other causes include SIADH, especially in patients with meningitis. SIADH is a volume-expanded state. Overhydration is potentially much more dangerous than dehydration. In this case, the patient demonstrated hypotonic hyponatremia with maximally dilute urine consistent with water intoxication. SIADH is water overload and not salt depletion. This leads to excess water elimination as dilute urine.

The record at N-2 documents “Foley draining lge amt dilute urine” again at 0425 hours, while N-1 of the record documents “Foley catheter emptied for 1200cc dilute urine” at 0450 hours that is consistent with conditions featuring osmotic diuresis, such as diabetes insipidus (“water diabetes”). It occurs in association with Na+ Disorders, primarily related to Na negligence, due to iatrogenic fluid overload.

The central causative mechanism in this case, involves a hyperglycemia-induced osmotic diuresis and resultant dehydration. Polyuria due to excess fluid intake and glucose-induced osmotic diuresis is common in patients with transient hyperglycemia. The hyperglycemia emanates from a commonly identified diabetogenic stressor, such as infection, which precipitates the onset of the syndrome, which in turn produces pseudohyponatremia commonly associated with hyperglycemia. Another is drug-induced hyperglycemia, which should not be overlooked in this case.

Polyuria has been observed in a severe case of GBS. Polyuria in GBS is multifactorial and would be partly due to a dysregulation of osmoreceptors. Besides dangerous cardiac manifestations, neuro-endocrine changes are also reported and could induce electrolytes and fluid balance impairments.

CAVEAT: Hyperglycemia can lower the serum sodium concentration by 1.6 mEq/L for each 100 mg/dl, giving rise to a false test. There is undoubtedly an involvement of metabolic derangement and neuronal injury in the detrimental effects of hyperglycemia. Hyperglycemia is particularly detrimental in ischemia/reperfusion.

Hyperglycemia is ALSO reported to trigger massive neutrophil deposition in brain following transient ischemia. If tissue invasion is mild, small areas of necrotic tissue resorption may occur, but if the bacterial invasion is massive, acute suppurative abscesses can arise.

A-15 documents the 24 hour IV fluid balance record, that between 1745 hours and 0200 hours was administered as follows: A-14 documents an ” IV gid prn”, meaning that fluid and medication rate of administration to be is given by IV as follows: 3.3 % dextrose (a sugar solution used in intravenous drips) and 0.3 % sodium chloride solution (referred to herein as “2/3 and 1/3?) @ the rate of 100 cc/hr, together with the medications, as evidenced at A-15.

The combination of 3.3% dextrose and 0.3% sodium chloride (known as 2/3 and 1/3) contains only 51 mmol/L of sodium. Outside of the body, the osmolarity of the solution is 269 mOsmol/L (sodium and dextrose combined). Once the solution is infused, however, the dextrose is rapidly metabolized, which leaves two-thirds of the solution (667mL) as electrolyte-free water and renders the solution extremely hypotonic. The patient will suffer a decrease in the osmotic concentration of the plasma which is now hypoosmolar to red blood cells and so water enters freely by osmosis and the cells swell and eventually burst, resulting in lysis of many red blood cells and the inability to oxygenate the brain, etc.

A red blood cell placed in a hypotonic solution (ie, pure water) bursts immediately (“hemolysis”) from the influx of water. Other conditions that can cause hemolysis include immune reactions, toxins and poisons.

A-20 documents a Sodium level of 144 with a reference range of 137-145 mmo1/L, being normal. Sodium is an electrolyte that helps with nerve and muscle function, and also helps to maintain blood pressure. Sodium circulates in the body fluids outside the cells. It is very important for maintaining blood pressure. Sodium is also needed for nerves and muscles to work properly. It is important to note, however, that hyponatremia more often represents excess of water than insufficiency of sodium. Lack of sodium is only very rarely the cause of hyponatremia, although it can promote hyponatremia indirectly. Notably, serum Sodium is lowered 1.6meq/L for every 100mg/dl glucose; hyperglycemia can lower the serum sodium concentration by 1.6 mEq/L for each 100 mg/dl as the high levels of glucose draw intracellular water into the extracellular space, giving rise to a false test.

Adequate sodium balance is necessary for transmitting nerve impulses and proper muscle function, and even a slight depletion of this concentration can cause problems.

Further, it is never appropriate to use the combination of 3.3% dextrose and 0.3% sodium chloride (known as 2/3 and 1/3) as “initial” fluid resuscitation in the dehydrated patient. Its use is limited to those who have severe hyponatremia unresponsive to isotonic saline boluses or who need concomitant fluid restriction. To restrict fluid resuscitation in an already dehydrated patient is outright stupidity, and constitutes an act of wanton and reckless disregard for human life. In addition, if there is reason to be concerned about impaired function of the brain, heart, or kidneys, it is always prudent to rehydrate more slowly. This empirically-derived approach minimizes the cerebral disturbances (e.g., seizures, cerebral edema) caused by fluid shifts that can occur if fluid is infused too rapidly. It needs to be clear that all guidelines regarding fluids and electrolytes are approximations that in no way can replace careful monitoring of the patient.

Hypotonic dehydration causes the amount of deficit to be overestimated by physical examination.

The record at A-15 documents a total IV solution + additives of 1000 cc TBA, (to be absorbed), documented by Nurse Bates at 1745 hours; with a 150 ABS (absorbed) by 1900 hours, documented by Nurse Ferguson, shows 150 cc absorbed over a period of 75 minutes; exceeds the rate of 100 cc/hr by 25%. Anything above the 100 cc/hr points to “overly rapid infusion” leading to overhydration or “water intoxication”, which mimics features of diabetes.

Solution + Additives of 850 cc TBA remaining at 1900 hours documented as ABS (absorbed) by 0200 hours, over a period of 7 hours, resulting in a “surplus” of 150 cc fluid, with an additional 1000 cc TBA, and NO further documentation with respect to IV monitoring.

A-19 documents a Lymphocytes count of 2.0 L, with a reference range of 20.0 to 50.0 which is extremely low. Initially, lymphocytopenia has been described in case reports concerning infectious emergencies such as toxic shock syndrome. Absolute lymphocytopenia has been reported as a predictor of bacteremia in medical emergencies, and is also used in the prediction of infectious emergency admissions.

Hyponatremia follows from a “surplus of water” due to Na negligence. Other evidence of fluid overload as indicated by “ascites” due to fluid build-up in the abdomen, evidenced at A-19, marked by a low lympocyte count. Irreparable harm can befall the patient when abnormal serum sodium levels are corrected too quickly or too slowly. Rapid correction of hyponatremia, even mild hyponatremia, risks neurologic complications (see Fluid and Electrolyte Metabolism:Osmotic demyelination syndrome).

A-20 documents a Sodium level of 144 with a reference range of 137-145, being normal. It is important to note, however, that hyponatremia more often represents excess of water than insufficiency of sodium. Lack of sodium is only very rarely the cause of hyponatremia, although it can promote hyponatremia indirectly.

Generally, Na should be corrected no faster than 0.5 mEq/L/h. Increase should not exceed 10 mEq/L over the first 24 h. Any identified cause of hyponatremia is usually treated concurrently. The record shows a complete absence of information with respect to “Water Refill”, suggestive of withdrawal or deliberate discontinuation with NO monitoring.

An association between SIADH and diabetes mellitus has also been reported; the basic fluid problem in SIADH is water overload and not salt depletion. Use of hypotonic fluids in presence of circulating ADH can causes free water retention resulting in hyponatremia. Other nonosmotic stimuli for the release of ADH include pain, stress, fear, gastroenteritis, hypoxia, positive pressure ventilation, trauma, and medications such as opioids.

Hyponatremia exerts most of its clinical effects on the brain. Brain volume is regulated by equal osmolality of extracellular and intracellular fluid. When extracellular osmolality decreases, water influx occurs in the brain resulting in cerebral edema due to electrolyte-free water moving into the brain cells. Cerebral edema is a condition where the brain's water content increases, causing the pressure inside the skull to rise.

The record at N-6 documents “IV infusing well”, suggestive of overzealous IV infusion. Be aware that rapid administration of hypotonic IV fluids can cause swelling of the brain cells, and increased intracranial pressure. Further, rapid correction of hyponatremia may result in brain dehydration, cerebral bleeding, demyelination, neurologic injury, or even death.

Circulatory overload can occur if IV is not regulated properly and IV fluids infuse too rapidly for the patient’s body to handle. Signs of fluid overload include tachycardia, elevated blood pressure, dyspnea and other signs of respiratory distress.

Correction of serum sodium that is too rapid can precipitate severe neurologic complications as a result of intracerebral osmotic fluid shifts and brain edema. This neurologic symptom complex can lead to tentorial herniation with subsequent brain stem compression and respiratory arrest, resulting in death in the most severe cases. The primary cause of morbidity and death is brainstem herniation and mechanical compression of vital midbrain structures.

Seriously ill patients always require accurate fluid balance monitoring because IV fluid also contains the medication(s). Rapid infusion may also lead to over-dosage. There are no further IV related entries on the record, either to indicate when or if the IV was discontinued, or to show that the rate of administration was being accurately monitored, or modified, suggestive of deliberate omission, or iatrogenic neglect.

The same record documents a “hard” IV site in the “R” (right) hand; clot formation due to irritation, of the vein from solution or medications is the most common cause of a hard IV site. The back of the hand has weaker veins.

Circulatory overload can occur if IV is not regulated properly and IV fluids infuse too rapidly for the patient’s body to handle. Signs of fluid overload include tachycardia, elevated blood pressure, dyspnea and other signs of respiratory distress.

Notably, Stemetil 10mg was added to the IV at 2030 hours. The drug is sedating and a potent vasodilator, which also crosses the blood-brain barrier. Patients are usually “volume expanded” prior to its use, resulting in neurologic derangement.

The record at N-4 documents the patient’s “transfer to ICU in respiratory distress” at 0320 hours, while record at N-3 documents a “congested oral airway” at the very same time, meaning congestion of the breathing passages. Obstruction of the air passages of the nose, mouth, or throat may also lead to difficulty breathing. Certainly the inability to breathe properly can be alarming, and many persons will immediately react with anxiety, fear, or panic.

The record at A-24 documents the mechanical charting of the patient’s vital signs that commenced recording at 0315 hours. It is interesting to note that the patient’s transfer to the ICU had not yet taken place, and that no prior attempt was made by any of the health-care providers to place the patient in the ICU prior to 0320 hours. It seems clear that the health-care provider had done too little too late, as evidenced by the records at N-9, N-10, N-11, including A-3, and A-21.

From the record as a whole, it is also clear that both doctors should have realized at the onset, from the severity of the patient’s signs and symptoms that they were faced with a critically ill young woman who was not responding to their questionable treatment. Those patients with severe disease who do not respond to treatment are labelled as having fulminant disease. They should ALSO have been acutely aware of the danger. Critically ill patients frequently have multiple physiologic derangements that come from a range of possible sources and they usually occur simultaneously.

N-5 of the medical record documents a gurgly respirations as evidenced by a “gurgly resps” at 0220 hours, a sign of constriction suggestive of thoracic trauma (patients are often in shock). The same record documents “deep and soaring and without constant jaw thrust”, such as associated with obstructive sleep apnea. Gurgling is a bubbling sound. It usually indicates upper airway obstruction from throat secretions, or presence of fluid in the airway. excessive pooling oral secretions due to Bulbar palsy

The record at N-4 of the Nurses’ Notes documents an “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. Dark, concentrated urine in decreasing amounts is also a prominant finding in patients with high blood sugar (hyperglycemia), including dehydration.

A-8 documents “family claims she had been pulling to the right over the last 4 or 5 days”, suggests hemiparesis - weakness, paralysis on one side of the body - sudden right hemiparesis due to a brain abscess marked by impaired muscle coordination manifesting as staggering and stumbling.

Right-sided hemiparesis involves injury to the left side of the person's brain, which is the side of the brain controlling speech and language. Aphasia - poor speech, for example, slurred speech.

A-8 of the related record documents “patient was unconscious with respirations of approximately 30 and laboured”, that is consistent with dyspnea, being difficult or labored breathing. Dyspnea is breathlessness due to high filling pressures and pulmonary congestion/edema, i.e. shortness of breath, a smothering feeling, inability to get enough air, and suffocation. Breathing may become labored and difficult; labored breathing is the hallmark of respiratory distress and respiratory failure due to paralysis of the diaphragm. Breathing is affected by weakening the muscles of the chest wall and diaphragm; in these cases, mechanical ventilation is required immediately. Dyspnea should always be taken seriously.

A-1 documents “plantars upgoing bilaterally”. Submit that the plantar reflex is a hallmark of the Babinski sign, a test for signs of disease process in the motor neurons of the pyramidal tract. Initial drowsiness, bilateral plantar responses, and quadriparesis, is strong clinical evidence of central involvement consistent with drugs or toxins that affect the basal ganglia, thalmus or brain stem. Drugs such as prochlorperazine can impact the pyramidal tract, so can infection.

The patient became apparently unresponsive, as evidenced at N-5, and went into respiratory distress, requiring ventilation for which she was transferred into ICU at 0320 hours, according to the record at N-3. The same record documents the time of the patient’s intubation by Dr. Jordan at 0325 hours, some 5 minutes later. What I take to be the Ventilation Record at A-17 documents the arrival in the ICU of the hospital’s ventilatory therapist, Helene Studholme at 0330 hours, after being “called in for patient requiring ventilation”.

From these records, it is clear that the ventilatory therapist was NOT present at the time of the intubation procedure because she did not show up until 5 minutes later. Submit, the intubation took place at an earlier time, such as 0320 hours.The record at A-24 documents a HR (heart rate) of 174 bpm at 0320 hours that is consistent with an awake intubation (any suspicion of difficulty intubating, for any reason), marked by panic with awareness (shock), resulting in an increased heart rate. To illustrate, the Vital Signs Record at A-24 documents a heart rate of 174 bpm at 0320 hours that is consistent with trauma, while the Ventilation Record seen at A-16 documents a heart rate of only 126 bpm within the same time frame, a significant difference, suggesting that the timeline for that event was in fact altered by the Ventilatory Therapist to conceal evidence of iatrogenic trauma related injury.

The Vital Signs Record is a mechanical record with a run time, while the Ventilation Record in this case is a handwritten account, marred by having been “rewritten”. Which method of recording is more likely to make scribe errors, or downplay an event by omission, or incorporate lies?

Additionally, there is nothing on record to suggest that anesthesia was given to prepare the patient for the intubation procedure and submit that nothing entered that ought to have been entered on the record can only infer “nothing done”. Also, for the record, know that the earliest indication of shock is an increase in heart rate, in this case the 174 bpm at 0320 hours evidenced at A-24.

Presentation of shock will depend on the aetiology but will usually be recognised by hypotension, decreased urine output, and clouding of consciousness. A compensatory tachycardia may or may not be present.

According to Dr. Jordan “the intubation proceeded uneventfully”, while N-2 of the record documents the ET (endotrachial tube) “pulled back 4 cm” (1.5748 inches) at 0425 hours. From that record it seems clear that the endotrachial tube had been malpositioned for almost one full hour before the error was discovered by one of the nurses, evidenced at N-2, as to infer negligence on the part of the Dr. Jordan, including failure on his part to identify an incorrectly placed airway in a timely manner. Both myself and the patient’s foster brother were present to witness that event. Endotracheal tube malpositioning into a mainstem bronchus or the esophagus may result in significant hypoxemia (inadequate oxygenation of the blood).

When an endotrachial tube is misplaced in the esophagus and misplacement is detected late, a compromise of the patient’s safety can be significant. Malpositioning of the ET tube can cause airway obstruction and may also result in tissue trauma and bleeding. Iatrogenic perforation is the leading cause of esophageal perforation.

A-12 of the medical record documents a blood pressure of 163/117 bpm at 03:20 hours that by 0345 hours had dropped to 85/58 bpm, following intubation, with an additional drop to 85/52 bpm by 0352 hours, over a span of some 7 minutes, as evidenced at N-2 of the Nurses’ Notes. Extremely Low .

A-17 documents “being suctioned for moderate amounts of coffee-ground emesis by RN” at 0330 hours. Gastrointestinal bleeding due to stress ulceration is also an important complication in critically ill patients. GI bleeding is a medical emergency that was basically ignored by the healthcare providers, in this case.

The physician’s Lab Work Summary at A-19 documents the charting of a course of Hematology and Coagulation. The same record documents a Fibrinogen level of 4.67 H (the normal range is 2.00-4.00). Fibrinogen plays two essential roles in the body: it is a protein called an acute-phase reactant that becomes elevated with tissue inflammation or tissue destruction. elevated plasma fibrinogen (hyperfibrinogenemia) levels induce a state of hypercoagulability. Serum fibrinogen levels in a safe range is &lt;300 mg/dL. An elevated fibrinogen level may also be seen with TRAUMA of any kind. with risk of cardiovascular disease and arterial and venous thrombosis.

Hyperfibrinogenemia (elevated fibrinogen levels in the blood) is notable.

A-19 documents a D-dimer test level of 1000 H. An increase in fibrinogen and d-dimer correlates with thrombotic activity suggestive of thrombosis. Thrombosis signifies the formation of blood clotting within vessels of the brain or neck. People who are suffering from a severe infection are more likely to develop dangerous blood clots, but inappropriate combinations of medications or treatment can sometimes be the worst offenders.

Changes in the haemostatic profile - prolonged activated partial thromboplastin time, shortened thrombin time, increased concentration of D-dimeres and thrombocytopenia suggest the development of disseminated intravascular coagulation, most likely due to influence of blood clotting factors secondary to dehydration.

A-19 also documents a Platelet count of 544 H with a MOD INCREASE. An elevated platelet count is known as thrombocytosis. Platelet aggregation and thrombi form because of the increased viscosity of the blood. This can result in decreased tissue perfusion and the development of disseminated intravascular coagulation (DIC). A disorder characterized by procoagulant substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders.

A-19 documents the aPTT (activated Partial Thromboplastin Time), a test used to determine the efficacy of various clotting factors used in the diagnosis of coagulation disorders documents the therapeutic range for heparin therapy at 60-100 seconds (23-35 is the normal). The time of that assessment was documented at 0400 hours. The aPTT is typically elevated in 90% of those with coagulopathy.

A-19 documents a “PLT ESTIMATE” – “MOD INCREASE” confirming an increase in platelet aggregation activity, blood platelets sticking together, indicating that blood thinners may be needed to prevent blood clots.
The Cardiac Index seen at A-18 documents the patient’s ventilation rate at 129 bpm (breaths per minute) at 0417 hours, with heart and breath rate increased. Increased heart and breath rate can suggest clinical insult, such as caused or worsened by medications, resulting in oxygen deprivation. The same record also documents the patient’s age at “55 years”, she was only 41 at the time of her death; can infer negligence, or even patient record swapping.

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”.Pale skin suggests decreased blood supply to the skin. Blood vessels in the body constrict to conserve blood in the body’s core, making you feel cold and your skin go pale.

Cool, dry skin can also suggest late sepsis. Patients progressing from sepsis to severe sepsis become profoundly dehydrated. The skin is the first place to be robbed of water, resulting in dry skin. The skin turns pale and cold .

Severe dehydration (loss of 10-15% of body fluids) is a life-threatening condition that requires immediate medical care.

Caveat - Sepsis causes profound hypotension. Sepsis refers to the presence of an infection, plus any two of these four criteria:

. Heart rate greater than 90 beats per minute

. Increased respiratory rate

. High or low white blood cell count

. Fever or low body temperature

. Visible symptoms of sepsis include nausea, vomiting and chills in the presence of an infection. The record speaks for itself.

The most frequent sites of infection leading to sepsis are the lung, urinary tract, abdomen, and pelvis. In up to 30 percent of patients, however, a definite source of infection most often cannot be identified. The course of the disease is unpredictable. Some patients quickly deteriorate, while others suffer from varying degrees of organ dysfunction or begin to recover.

Hallmark of infection is fever; however, temperature can vary with severity of sepsis, typically 37.2°C or &lt;36°C can be indicative of severe infection.

Other signs that can also suggest sepsis are tachycardia, tachypnea, hypotension, an identified source of infection, and toxic appearance. Nonspecific but contributing findings include leukocytosis, neutrophilia, and toxic granulations.

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”. Gravol (dimenhydrinate) is contraindicated in lung disease and has also been reported to “mask the presence of underlying organic abnormalities and/or the toxic effects of other drugs”. Dimenhydrinate may mask the signs of an acute abdomen. Since dimenhydrinate is capable of masking ototoxic symptoms, use with caution in conjunction with certain antibiotics that may cause ototoxicity; these medicines may mask symptoms and interfere with treatment.

The record at A-8 and A-9 documents “Medi-Vac team were due to arrive at 0435?, while the Ambulance Call Sheet documents “call received at 0620? hours, a significant difference.

The record at N-7, documents “pulses X 4 good”; head and neck OK; chest OK; “abdomen OK”; pelvis OK; extremities OK. From the record this is an absolute falsity.

A-1 of the record also documents “she died several days later with numerous metastatic lesions to her brain”. According to her death certificate, Arlene Berry died May 24th of 2000, the very same day she was transferred out to Sudbury. As to the cause of death, according to a Dr. Sauve in Sudbury, she died “meeting brain death criteria”.

No pathalogical reason was given for the declaration of brain death. No process of exclusion was undertaken without which a diagnosis of brain-death should never have been considered. NO explanation was offered to explain what can only be construed as a “fixed drug erruption” on the deceased’s right cheek. following her return to Kirkland Lake, Ontario, after her demise.

It is believed that Arlene Berry’s death was deliberately provoked and that her eyes were taken by Drs. Sauve, and Adegbite at the Sudbury Regional Hospital, upon remote third party consent via her foster brother acting as a family contact, who was notified by phone. utilizing deception to obtain that consent, by-passing permission from Arlene Berry’s immediate family, ie, her de facto common-law spouse and her children.

From the information at hand, it seems clear that Drs. Sauve and Adegbite sought to open the way, under misleading conditions (influence of drugs, and metabolic disturbances) to organ donation from brain death. The diagnosis of brain death allows organ donation or withdrawal of life support. These doctors allowed this patient to die to achieve their nefarious ends due to hospital constraints.

Only unscrupulous clinicians might withhold medical treatment and attempt to influence the family in inappropriate ways such as this. Indeed, the fraudulent taking of the patient’s eyes in the manner in which it was done can only be construed as theft. The patient’s death can only be viewed as a medical homicide.

Certifying brain death to cover-up medical blunders or to increase organ donations constitutes complicity.

Arlene Berry’s remains was returned to Kirkland Lake several days after family had been notified of her death only hours after her transfer Sudbury Regional Hospital On seeing the deceased, her eyes were “sunken in appearance”, with swelling and distortion of the face, eyes, and lips, as was the case, marked by a rash-like redness resembling a sunburn with “blistering” wrinkles in the skin on her right cheek, in the area just below the right eye, consistent with a delayed hypersensitivity reaction, or fixed drug-eruption, evidenced by all who attended Arlene Berry’s viewing at the Monette-French Funeral Chapel in Kirkland Lake. Skin sensitivity is also common in acute parasite infection: rashes, eczema-like conditions, and even serious eruptions have been reported in the literature.

The term ‘sarcoidosis’ was coined in reference to the skin eruptions that occurs as a consequence of the disease.

At a first meeting with the coroner held at the OPP Detachment in Kirkland Lake sometime in July of 2001, Dr. Barry A. McLellan, who was the Regional Supervising Coroner for northeastern Ontario at the time admitted to family that there was “no evidence on record to suggest matastasis”, meaning NO evidence of spread of cancer.

At a subsequent meeting between family and Dr. McLellan, he provided us with a view of a CT scan that was purportedly done in Sudbury, Ontario at the time Arlene’s death on May 24thy of 2000, although I suspect it may have been done following withdrawal of llife support. It .shows lesions but these are nonspecific The pathogenesis of these yet undetermined lesions remains unclear but serious infection and/or a metabolic disorder seems the most plausible pathological factors. Appearances of lesions in CT with focal and/or multifocal contrast enhancement are frequently mistaken for brain tumors.

Parasitic cysts of any origin may mimic primary or metastatic brain tumor(s). Symptoms may develop slowly, over a period of 2 weeks, or they may develop suddenly

http://www.nlm.nih.gov/medlineplus/ency/article/000783.htm

Based on the patient’s belated CBC’s, the lesions are consistent with collections of purulent exudates (pus producing bacteria), suggested by an elevated Neutrophil count in the presence of an elevated WBC count, and/or pockets of pooled blood, as suggested by an elevated Fibrinogen in the presence of an elevated D-dimer, a hallmark of thrombus formation, ie., blood clots. The enhancement is obviously due to infection, or blood pooling, or both.

Saddly, Arlene Berry died suddenly and unexpectedly on the 24th day of May, 2000. Total time lapse 24 days; mean 3 weeks , or just under 4 weeks following radiotherapy. That she had mentioned a cyst/infection should be born in mind.

No autopsy was performed, as I understand it, because the patient died “while under the care of a physician”. No appropriate period of observation and/or trial of therapy was ever undertaken. In fact, Arlene Berry was rushed to her death within five and one-half hours of her departure from the Kirkland and District Hospital to Sudbury Regional Hospital, some 210 miles away.

One might ask how much time did these medical dolts actually spend assessing the patient before taking away her life support? The speed at which they acted to hasten this death is nothing short of criminal. Although many conditions can mimic brain death clinically upon examination, without excluding them you will KILL a person by homicide, or criminal negligence, despite the reversibility of brain damage.

Brain death is defined as the irreversible cessation of function of the entire brain with three specific criteria: 1) coma, 2) absent brainstem reflexes and 3) apnea. In addition to these clinical criteria, there are important prerequisites: 1) NO drug related intoxication or poisoning, 2) NO core temperature greater than 32 degrees Celsius, 3) clinical or neuroimaging evidence of acute central nervous system catastrophe and 4) absence of confounding medical conditions such as severe electrolyte, acid-base, or endocrine disturbances. From the record it is clear that none of these protocols were adhered to.

As a safeguard in determining brain death a number of tests need to be carried out every 6 hours and recorded. The physicians performing this determination must not be part of a transplantation team. In some cases, 48 to 72 hours or more is required to evaluate brain death and a repeat examination with observation up to an additional 24 hours is sometime needed. The length of time between serial examinations to declare brain death varies marginally from 6 to 72 hours. Notably, severe cases of GBS may mimic brain death.

http://pmcc.web-t.cisti.nrc.ca/articlerender.cgi?accid=PMC2686862

Further, the Sudbury doctors involved were a part of an organ harvesting and transplantation team. It was Dr. Sauve who, utilizing deception, sought to obtain permission from a remote third party to obtain the victim’s eyes, without immediate family knowledge or consent.

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. The solitary lesion is also consistent in appearance with a 1 cm amebic brain abscess, after capsule formation in the early stage of abscess development. Amebic brain abscesses may be single or multiple. An elevated white blood cell count is usual with a marked increase in neutrophils.

http://www.ncbi.nlm.nih.gov/pubmed/20578451

The regions of the CNS where lesions may be observed are the midbrain, occipital lobe, and posterior fossa. Rupture or leakage of a cyst contents into a ventricle or subarachnoid space may produce an epidymitis or meningitis respectively. Further, a single capsule can rupture resulting in the formation of multiple abscesses.

Know that the occipital lobes interpret vision. 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, or pyogenic brain abscess, usually of bacterial or parasitic origin.

Had the lesion been a recent tumor, there would have been onset visual misperception in half of one or both visual fields, with visual impairment and subsequent loss of vision with evolution, prior to hospital admission. That did not happen. Know that even multiple brain abscesses may not cause focal deficit to suggest their presence. Further, with multiple abscesses or infection the meninges typically show a purulent exudate that obscures the sulci making radiographic appearance of microabscesses less visible, hence they are “not well opacified”

Non-neoplastic demyelinating processes of the brain with ring enhancing lesions and mass effect on MRI imaging, mimicking malignant brain tumors, are also a rare phenomena that was never considered. The radiologic appearance of demyelinating pseudotumors as contrast-enhancing masses that mimic tumor(s) is well documented, ie., “tumor-like” masses of demyelination, or “granulocytes that mimic brain tumors”.

A brain abscess is generally caused by bacterial spread from an infection elsewhere in the body. Morbidity due to a brain abscess generally results from brain herniation due to mass effect, often the result of iatrogenic neglect, or substandard care, or both.

NOTABLY, nothing was done to reduce symptoms OR the likelihood of cerebral herniation.
No autopsy was performed in this case. Further, a family request for a formal inquest was also denied. Dr. McLellan concluded that Arlene Berry had died of “natural causes” suggestive of metastatic CA of the brain with multiple brain tumors after eliciting an opinion from one of his fellow colleagues believed to be associated with the Sunnybrook Health Sciences Centre, where McLellan spearheaded the North Telehealth Network. The medical record of Arlene Berry for May 23rd and 24th of 2000, tells a very different story from the opinion postulated. One might ask, why was so much evidence to the contrary ignored?

Misdiagnosis and autopsy studies: One useful way to detect misdiagnosis is to perform an autopsy, and then compare the original diagnosis with that found at autopsy. Various studies have found major differences, with discrepancy rates as high as 40% in the Medical ICU (CHEST, February 2001). This rate of 40% in the ICU is undoubtedly higher than the rate for general medicine because of the difficult and often multifactorial nature of serious ICU cases. Unfortunately, autopsy rates are declining for various nefarious reasons and the opportunity to measure misdiagnosis in this way is purposely reduced.

Eleven percent of mass lesions in cancer patients are not metastases; mass lesions that can masquerade as brain metastasis include abscess(20%) and granuloma (less common and mostly associated with myco-bacterial, fungal, or parasitic infection); parasitic, and indolent bacterial infections have been known to occasionally mimic cancer.

The commonly observed deficits in CNS infection include weakness on one side of the body (hemiparesis), impaired speech production (dysphasia), visual field deficits (may or may not be present), and an inability to smoothly coordinate muscle movements, such as during walking (ataxia), which would cause a person to pull in one direction or another when walking,

Brain Tumor is often considered in the diagnosis of lesions demonstrated on brain computed tomography (CT) and/or magnetic resonance imaging (MRI). Brain tumors usually show abnormal densities on CT or altered signal intensities on MRI, mass effect, and sometimes contrast enhancement after the intravenous administration of contrast material. Lesions with these features, however, are not always brain tumors and establishing the diagnosis of a brain tumor is not always a straightforward process. Cerebrovascular diseases, demyelinating processes, inflammatory or infectious diseases and other miscellaneous diseases can show similar imaging findings.

Many non-neoplastic neurological diseases can mimic brain neoplasms on neuroimaging or on histological examination, including multiple sclerosis, stroke, pyogenic abscess, toxoplasmosis, tuberculosis, cysticercosis, fungal infections, syphilis, sarcoidosis, Bechet’s disease, radiation necrosis, venous thrombosis, Guillain Barre syndrome and others. Multiple intracerebral hematomas can also mimic brain metastases. West Nile virus encephalitis mimicking central nervous system metastases from small cell lung cancer is reported in the literature.

Patients with a diagnosis of primary or metastatic brain tumor(s) associated with a CNS event should have a meticulous review of their history for other possible causes, especially iatrogenic causes.

The investigation and analysis of this case has been ongoing for most of 13 years with everything pointing to possible Guillain-Barré syndrome (GBS). Although brain death mimickery is not an acute finding in sarcoidosis or amoebiasis, it is with GBS, which  mimics brain death.  For the record, an association between neurosarcoidosis and Guillain-Barré polyneuropathy is reported in the literature.

That botulism may also mimic the symptoms of other diseases, including brain death, and especially diseases characterized by muscle weakness needs always to be kept in mind. A noteworthy diagnostic dilemma which may mimic GBS is botulism, and meningitis, encephalitis, Guillain-Barré syndrome, and botulism remains undeniably the presentation in this case. In fact, the uncommon Miller-Fisher variant of Guillain-Barré syndrome resembles Botulism. The symptoms of certain food poisoning organisms can resemble meningitis. Botulism may also resemble a dysentery syndrome, or even be confused with Guillain-Barre syndrome, myasthenia gravis, drug reactions, stroke, or nervous system infection, intoxications (e.g. carbon monoxide or atropine), or shellfish poisoning. Sepsis is another.  "Botulism is technically a illness-causing poison, but it masquerades as a disease (appearing to be a bad version of dysentery)..."   I have to ask, is there a possible common denominator here?

http://www.dandwiki.com/wiki/Botulism_%283.5e_Disease%29

http://medical-dictionary.thefreedictionary.com/botulism

http://www.guillain-barre.co.uk/condition-heavy.php

For the record, meningoencephalitis, from Greek: meninges- membranes; enkephalos brain; and inflammation is a medical condition that simultaneously resembles both meningitis, which is an infection or inflammation of the meninges, and encephalitis, which is an infection or inflammation of the brain consistent with certain forms of neurosarcoidosis whose pathogenesis involves formation of inflammatory lesions known as a granulomas, also consistent with certain forms of amoebiasis (known as invasive or fulminant amoebiasis).

About 90% of infected persons are asymptomatic. There are two basic types of amebiasis: intestinal and extraintestinal disease, which may exist simultaneously.

 http://www.ncbi.nlm.nih.gov/pubmed/21510240

Meningitis and encephalitis are usually caused by viruses or bacteria. Less commonly, encephalitis can result from a parasitic infection, such as PAM, or it may be a complication of other infectious diseases.

Questionable Opinion:

The anonymous author of an opinion sought by the coroner’s office (whose signature was erased) perceives himself to be expert in his field. Believed to be a neurosurgeon, perhaps the very same one who attended to Arlene Berry in Sudbury, this so called doctor is obviously lacking in diagnostic thoroughness. The bald truth is that specialists in a given field are not always expert in that field. In this case, his opinion remains unsubstantiated. He failed to provide any evidence whatsoever which might support a finding of metastatic CA of the brain. Further, a paltry CT scan does NOT provide conclusive proof of metastatic brain tumors. For that it takes a biopsy and in this case that was never done. Therefore the true nature of the lesions were never established. Nor does a CT provide conclusive proof of brain death. In fact the author who rendered the opinion suggesting metastatic cancer is pretty much off-the-wall; what one might expect from a “hand-picked, self-interest cash for comment” shill, or someone to be equated with a first year medical student whose opinion is highly questionable to say the least. The expert opinion even comes with a “disclaimer”.

The nameless author admits that his opinion “does not take into account all the facts and circumstances surrounding the patient’s death”, actually says it all since such a disclaimer can only raise doubt about the accuracy of the opinion rendered. The author bases his opinion on assumption, while ignoring the facts. Obviously he did not take the time to study the patient’s flawed medical record. Instead he opted to tailor or lard his report to justify the opinion that was, in his opinion , being sought by Dr. McLellan for the sake of expediency. This infers a blatant attempt by all concerned to obfuscate the truth.

A finding of possible meningitis with abscess of the brain and/or multiple intracerebral hematomas would have given more credibility to his opinion. In fact, some of the opinion expressed by the nameless author could also be used to support a finding of meningitis.

There is absolutely nothing on record to support a finding of metastatic cancer of the brain, apart from a paltry CT, which offers absolutely NO evidence to support it.

For the record, CBC is usually elevated in meningitis and there is initially a neutrophil predominance; polymorphonuclear leukocytes often predominated early in the course of infection.

Rapid deterioration is an invariable accompaniment of an untreated condition, in this case, an undiagnosed case of fulminant GBS with overlapping meningitis, in which rapid progress of the disease may actually be displaying a pronounced “blood-brain barrier breach”, characterized clinically by “rapid evolution”, the result of totally inappropriate treatment and/or medications which can breach blood-brain barrier integrity. Further, breakdown of the blood-brain barrier usually precedes inflammatory demyelination.

GBS is often associated with cerebrospinal meningitis and encephalitis. Coma in GBS is rare and is the symptom of cerebrospinal meningitis and encephalitis. The clinical manifestations of this condition included areflexia in the cranial and spinal nerves as well as apnoea. Cisterns may contain pus in cases of meningitis or other inflammatory conditions, such as sarcoid, or demyelination.

Although it is clear that Arlene Berry was transferred to Sudbury with ventilator support, and although Drs. Jordan and Spiller were aware of the need for emergency care and life support, after ordering it, they canceled it, using the secretive “no code” (Code 0) endorsement as a pretext for evoking a declaration of death and in fact waited for the patient’s death.

Within a few hours following her transfer from the Kirkland and District Hospital to the Sudbury Regional Hospital, Arlene Berry was declared as having met with ‘brain death criteria’ , while under the care of Drs. Stephane Sauve and Andrew Adegbite.

Arlene Berry's remains were kept in Sudbury for several days prior to being returned to Kirkland Lake. Yet, NO autopsy was ever performed.

Withholding life sustaining treatment from an “undiagnosed” patient with concurrent hyperglycemia, hypokalemia and electrolyte abnormalities in combination with a severely paralyzed motor function and who is under the influence of sedative hypnotic and tranquilizing agents is of questionable legality. Death results from respiratory paralysis and subsequent asphyxiation. Brain death is what happens when ventilator support is discontinued.

Brain death: resolving inconsistencies in the ethical ..

Turn off the respirator and in the natural course of affairs the patient dies from lack of oxygen.

To practice euthenasia by withdrawing life support to a critically ill patient is a medical homicide; to kill or destroy by preventing access of air or oxygen. An act of active euthenasia consists of killing someone; to do acts causing death, or by choosing not to act is also an act, which determines the course and the outcome of events. Turning off a respirator is a form of passive euthanasia that is practiced by doctors with a family’s consent. In this case, no such consent was ever given.

To allow or hasten a patient’s death to cover-up error or negligence or to obtain organs is reprehensible. It is nothing short of murder since such an act or omission which causes death carries the “intended” consequence of the act or omission, hence, the “mens rea”, or criminal intent.

In Canada and the United States, amebiasis - a source of infectious cysts, is most often found in immigrants. It also is found in people who have traveled to or who have come into contact with people from developing countries and in people who live or work in institutions or hospitals that have poor sanitary conditions, which pose health issues for all concerned. Some people, including doctors can be deadly parasite carriers and not even know it.

Further, many immigrant doctors who come to Canada have very low qualifications. Many of them have been exposed to malaria, parasites and many unfamiliar infectious diseases such as the amoebae (parasitic) and also pose public health risks from a variety of other emerging infectious diseases. Many Canadian doctors find it hard to keep abreast of medical trends in foreign countries

Also, know that adenocarcinoma and amebic cysts present similarly as an “area of consolidation”. Presentation as a pulmonary nodule mimicking lung cancer is also common. Routine bacterial cultures are usually “NEGATIVE” for pathogens, showing No Growth, as in this case.

Further, a change in the bacterial flora caused by a secondary bacterial (aerobic?) infection or the use of certain antibiotics may induce conversion from nonpathogenic to the active state (pathogenic) which causes clinical disease.

Notably, certain combinations of medications, such as penicillin and sulfa-based anti-biotics can also cause the body’s immune system to react by overstimulation, steering the body’s already exhausted immune system, and/or volume depleted patient into dangerous waters; the very same process by which Guillain Barre syndrome (GBS) may also be triggered. Cipro and Septra DS have been implicated high on the order of major offenders in drug-induced GBS.

Dr. de la Rocha immigrated to Canada from Mexico where he graduated from the National Autonomous University of Mexico. Mexico is a hotbed for parasites and unfamiliar infectious diseases , such as amebiasis, a source of infectious cysts. Iatrogenic infection is influenced by factors like poor sanitation and hygiene, e.g., external inoculation with contaminated hands, surgical gloves, instruments, etc., during or following surgery.

CAVEAT: Mexico is a hotbed for amoebic infection (amebiasis ), a source of infectious cysts.

In Canada and the United States, amebiasis is a source of infectious cysts, most often found in immigrants. Further, many immigrant doctors who come to Canada have very low qualifications. Many of them have been exposed to malaria, parasites and many unfamiliar infectious diseases such as amebiasis. Amebiasis is also found in people who have traveled to or who have come into contact with people from developing countries and in people who live or work in institutions or hospitals that have poor sanitary conditions, which pose health issues for all concerned.
 

Iatrogenic infection is influenced by factors like poor sanitation and hygiene, e.g., external inoculation with contaminated hands or surgical gloves, instruments, etc., during or following surgery, or other medical testing/procedures.

Multiple abscesses are also frequent in Mexico, where parasitic intestinal infections are multiple infections that constitute approximately 40% of analyzed individuals in which it is possible to detect more than one pathogen together with commensal parasites that are an indicator of fecalism.

Although there are occasional outbreaks in Canada, North Americans sometimes bring the bug back with them after trips. In Canada, amoebic infection is mostly encountered in small patches of population that have migrated from endemic areas.

Dr. de la Rocha is suspected of involvement in experimental virology, parasitology and/or of being the carrier, transmitter or purveyor of an infectious disease, such as the amoebae. This rogue doctor is no stranger to controversy. In April 1993, he received a suspended sentence, three years probation and a six-month suspension of his medical licence for his role in the October 1991 death of a 68-year-old lung cancer patient. He admitted dosing her with a noxious substance, potassium chloride, as well as morphine. One might ask, what motivated this unscrupulous physician to kill one of his patients in the first place? Perhaps the embarrassment of having had a history of fecalism associated with asymptomatic carriage of amoebic dysentery and passing it an unsuspecting patient ? A ''Virus in Stealth'' to help kill cancer cells ? How about an experimental "Trojan-horse" cancer therapy (genetically engineered parasite whose behavior mimics cancer ) ?

http://www.halfbakery.com/idea/Treat_20Cancer_20With_20Parasites

Dr. de la Rocha had a propensity for selective treatment, including a criminal past history of euthanasia. Since bringing this issue to light, de la Rocha has since moved from Timmins to Markham, Ontario, where is is now practising colonoscopy.

 

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