"Truth Cannot Live on a Diet of Secrets Withering
Within Entangled Lies" H. Michael Sweeney

The Arlene Berry Case

Updated June 22, 2008

When dealing with truth, liars and suppression of truth, or where a crime involves a conspiracy, or conspiracy to cover-up, accuse those guilty of the later freely. They (both those deliberately seeking to lead you astray, and those who are simply foolish or misguided thinkers) generally run for cover when thus illuminated.

Ontario Doctors Exposed!!!


Beware of Ontario's unscrupulous health care system and its illicit trade in body parts and how/why  some doctors may murder you to get them....

How unscrupulous doctors exploit medical complications!

  There is a public interest in knowing how Arlene Berry came to her death and how her healthcare providers are implicated.

 

Arlene Berry  was murdered May 24th of 2000 on the order of Dr. Edward Henry Jordan to cover-up medical stupidity. He treated her over the telephone, unseen, while sitting at home watching TV. He ordered a brain damaging neuroleptic drug following administration of an opiate narcotic in the face of undiagnosed and untreated  medical conditions, resulting in catastrophic decline.

 This is a case where the negligent combined administration of morphine and prochlorperazine, resulting in  "conscious sedation" was used to masker and exacerbated an atypical presentation of Guillain-Barré syndrome (GBS), a rare but reversible disorder of the CNS that affects the nerves in the body. No diagnosis was made and the patient was inappropriately taken off mechanical ventilation and declared as having met with brain death criteria within a very few hours following her hospital transfer from Kirkland Lake to Sudbury, in the province of Ontario. Only 41 years of age, Arlene Berry died a tragic, horrific, and senseless death in the face of treatable and potentially reversible conditions, for which I hold all of her healthcare providers criminally responsible. 

Ropper, Wijdicks and Truax, 1991, report that the average age of onset is 40 years.

 Arlene Berry died unnecessarily, the victim of a drug induced nightmare of unprecedented magnitude.

 

Introduction

Guillain-Barré syndrome is a disorder in which the body's immune system attacks part of the peripheral nervous system.

The first symptoms of this disorder include varying degrees of weakness or tingling sensations in the legs. In many instances, the weakness and abnormal sensations spread to the arms and upper body. These symptoms can increase in intensity until the muscles cannot be used at all and the patient is almost totally paralyzed. In these cases, the disorder is life-threatening and is considered a medical emergency. The patient is often put on a respirator to assist with breathing. Most patients, however, recover from even the most severe cases of Guillain-Barré syndrome, although some continue to have some degree of weakness.

A person with GBS may sometimes feel funny sensations in their skin, or tingling— this is because the nerves that transmit messages about sensation are not working properly.

 

If the injury to the peripheral nerves, including respiratory nerves, is accompanied by facial nerve paralysis, the clinical picture resembles the neurological condition detected in brainstem death.

The disorder can develop over the course of hours or days, or it may take up to 3 to 4 weeks.

Guillain Barre Syndrome can "mimic" almost any neurological disease process, including Brain Death .. effectively allowing doctors to 'cover-up' their medical mistakes and unsuspecting patients to proceed to organ harvest while in a total state of awareness,  under guise of having met with "brain death" criteria.

This paper represents a rare case of wanton and reckless disregard for human life on the part of several   nurses, and medical homicide (or liability murder) on the part of several doctors, with an attempted cover-up on the part of all concerned. In the very minimum, all of the doctors and nurses involved herein could potentially find themselves facing charges of criminal negligence causing death,  or murder, conspiracy notwithstanding.

A murder is the the unlawful killing or causing the death of another human being, with malice aforethought. Malice aforethought can be express, or implied by evidence, or by the facts, as in this case. 

 

The facts of this case have been taken from the deceased's medical record  from the Kirkland and District Hospital. A very small part of the information contained herein comes from observations made by the family of the deceased.  Virtually all of the information presented, with the exception of a few personal observations made by myself and based on the extensive research done, is now  a matter of public record.  

The allegations of negligence and homicide from which an inference can be made are mine alone and are indeed supported by the FACTS of the case, and by  evidence based supporting data. This is a true story and the case remains an ongoing private investigation. The implications of the findings are so profound that, according to a hospital insider, Health Canada  has issued a "gag-order" in an effort to save face (with so many doctors and nurses accused of wrongdoing), a blatant attempt not only to prevent the media from becoming involved, but also as a means to deny justice.

In my opinion the health authorities have also insinuated themselves into a conspiracy or party accessory (after the fact) to a medical homicide. These political and ministerial thugs, attached to the public purse,  including the sinister College of Physicians and Surgeons of Ontario and their corporate counterparts seem to think that they and the medical professionals they seek to shield are all above the law. In regards to their efforts to 'gag' the internet, it will never happen.

Published under a wide variety of titles internationally, the Arlene Berry case stands as a testament to what can only be construed as widespread corruption in Ontario's healthcare system.

 

Guillain-Barré Overlap Syndrome

Guillain-Barré syndrome (GBS) is a group of autoimmune syndromes consisting of demyelinating and acute axonal degenerating forms of the disease. Axonal neuropathies have multiple causes. Nerve conduction study helps differentiate the heterogeneous subtypes.

Guillain-Barré Syndrome is a frightening and disabling disease which strikes suddenly, sometimes with devastating effect. Symptoms typically progress over a period of a few days and are usually at their worst two weeks after onset.

 

Symptoms of Guillain-Barré get worse very quickly. It may take only a few hours to reach the most severe symptoms. Patients are paralyzed by the illness, but mentally alert and fearful.

GBS is a prodromal malaise.  In medicine, a prodrome is an early symptom indicating the development of a disorder or disease,  indicating that an attack is imminent.  For example low-grade fever, ill feeling,  anorexia (lack of desire to eat), and chills, are all part of the prodrome for the Guillain-Barré syndrome.  The prodrome may follow 12 to 24 hours of low-grade fever, a generally ill feeling, and abdominal or respiratory symptoms, but the beginning of symptoms is usually abrupt, marked by loss of appetite, dizziness, vomiting, and constipation. GBS frequently follows a flu-like illness. Several disorders, such as acquired hypokalemia, myasthenia gravis, periodic paralysis, and poliomyolitis, have symptoms similar to those found in GBS.  Many disorders secondary to GBS have also been implicated.

Evidence Based Medicine SEARCH FINDINGS:  "Guillain-Barre syndrome is an acute, inflammatory, postinfectious polyneuropathy marked by a prodromal malaise with vomiting, headache, fever and limb pains is rapidly surmounted by a progressive and ascending paralysis. This can lead to respiratory dysfunction, and as such, the acute presentation can be a neurological emergency."   For example, malaise, headache and anorexia (lack of desire to eat) are part of the prodrome for the Guillain-Barre syndrome (GBS). 

Prodromal Phase: This is the period of time (could be hours, days, months or even years) when a medical illness is in its earliest stages. 

Guillain-Barré syndrome (GBS) is an autoimmune disorder. It occurs when the immune system accidentally attacks the nerves in the lower back, stripping them of their protective myelin sheath. This causes these long nerves to 'short circuit' and cause changes in the sensation and function of the body.  Paralysis results because nerve signals can't pass to muscles. Autoimmune diseases run the gamut from mild to disabling and potentially life threatening. Nearly all affect women at far greater rates than men.

Guillain-Barré syndrome (GBS) is an eponym for a heterogeneous group of immune-mediated peripheral neuropathies. Molecular mimicry  is implicated. A feature common in all GBS variants is a rapidly evolving polyradiculoneuropathy preceded by a triggering event, most often an infection.  GBS generally manifests as a symmetric motor paralysis with or without sensory and autonomic disturbances.

A special form of the syndrome is the Miller-Fisher syndrome (MFS) in which signs of the cranial nerve deficit dominate in the first phase of the disease.  Also known as acute disseminated encephalomyeloradiculopathy, MFS is very rare.

 

 

Autoimmune diseases tend to occur together.  Some examples of autoimmune diseases include lupus, Type 1 diabetes, multiple sclerosis, Guillain-Barré  syndrome, and many other conditions.

Guillain-Barré syndrome (GBS) is a rare but reversible neurological disorder that occurs when the body's immune system attacks the peripheral nerves in the body. This is known as an autoimmune disease and can also be triggered by a recent medical procedure, flu-like illness, or stomach infection. As the immune system fights off infection or illness, it mistakenly attacks the peripheral nerves.

Guillain-Barre Syndrome typically follows a respiratory or gastrointestinal illness, immunization, trauma, or metabolic insult.

 

The term "autoimmune disease" refers to a varied group of more than 80 serious, chronic illnesses that involve almost every human organ system. It includes diseases of the nervous, gastrointestinal, and endocrine systems as well as skin and other connective tissues, eyes blood, and blood vessels. In all of these diseases, the underlying problem is similar--the body's immune system becomes misdirected, attacking the very organs it was designed to protect.

 

Because you have one autoimmune disease, you may have a problem with your immune system, making you more susceptible to other autoimmune diseases.  Some patients have multiple autoimmune disorders with symptoms and diagnostic criteria that can and will invariably overlap.  In fact, both GBS and diabetes (especially hyperglycemia) share a commonality with neuropathy, infection, coagulopathy, and SIADH,  observed in each of these disorders,  suggesting a shared mechanism, or similar underlying pathological mechanisms. 

It is always possible to have two or more conditions or diseases rather than just one. For many diseases, there are usually other diseases that are related to it or associated with it.  The first disease is a risk factor for the second. Two conditions may be caused by the same underlying condition (i.e. a third underlying condition): for example, diabetes and hypertension may be related due to underlying metabolic syndrome.  For thie same reason, GBS may therefore overlap with other related disorders, including diabetes.

Ropper, Wijdicks and Truax, 1991, note acute illness of any sort precedes Guillain-Barré  syndrome in approximately two thirds of patients, and that incubation of the syndrome may be up to 6 weeks. But the average time between acute illness and onset of GSB is 11 days (Ropper, Wijdicks and Truax, 1991).

 

GBS is usually associated with prolonged length of ICU and hospital stay and requirement for rehabilitation, with significant use of healthcare resources and cost implications is of itself sufficient motive for medical homicide.

Presenting symptoms of GBS include 'flu-like' symptoms, absence of fever at onset, pain (especially back pain), paresis of the extremeties, cranial nerve compromise, ataxia, and associations of different types of symptoms, including stroke-like symptoms, or overlaping spectrum of unusual presenting symptoms and/or atypical variants, frequent respiratory impairment, usually following a history of infection(s), especially gastrointestinal or respiratory infection from 1-3 weeks prior to onset of weakness, tingling and/or odd sensations with no energy, dizziness and/or imbalance, facial paralysis, dysphasia or dysarthria, difficulty swallowing, fluctuations of heart rate, sinus tachycardia (>90/min), arrhythmias, labile blood pressure, hypotension or hypertension, malaise with nausea qnd vomiting, urinary and/or rectal dysfunction, variable temperature, inappropriate antiduretic hormone occurs in some patients, many different abnormalities may also be seen, e.g. 2nd and 3rd degree AV block, T-wave abnormalities, ST depression, QRS widening, and a variety of rhythm disturbances, aseptic meningitis, and coagulopathy such as  deep vein thrombosis and/or sinus thrombosis, suggestive of blood clotting. Time to development of deep vein thrombosis (DVT) or pulmonary embolism (PE) varies from 4-67 days following symptom onset.

Sensory loss if present is usually minimal. Oculomotor paralysis characteristic in the Miller Fisher variant may also be observed. The connection with GBS comes because some GBS patients develop paralysed eye muscles too. Consequently, Miller Fisher and Guillain-Barré syndromes may overlap.

Coagulopathy in GBS may present with an elevated fibrinogen level and is typically elevated at presentation. Many secondary complications that follow GBS include deep vein thrombosis, anemia, and mild to moderate migraine attacks which may include  a wide range of adversities. A higher than normal fibrinogen level in the presence of D-dimer is the hallmark of thrombosis, indicating that blood thinners may be needed to prevent blood clots.

"Fisher syndrome, a brainstem encephalitis, mimics brain death".

 

Miller Fisher syndrome  is a rare, acute polyneuropathy.  Miller Fisher Syndrome (MFS) is a syndrome of ophthalmoplegia, ataxia and areflexia associated with acute idiopathic ophthalmologic neuropathy, manifests as a descending rapidly developing but reversible paralysis, proceeding in the reverse order of the more common form of GBS. It usually affects the ocular muscles first and presents as ophthalmoplegia, ataxia, and areflexia.  Physical findings include delayed pupillary light response, sinus tachycardia, arrhythmia, and orthostatic hypotension. In fact,  Miller-Fisher variant of Guillain-Barré syndrome resembles botulism. Like botulism, MFS preferentially strikes cranial nerves, but with the additional sign of ataxia. Fisher syndrome, a brainstem encephalitis, mimics brain death.

MFS is a rare focal encephalitis of the brainstem characterized by cranial nerve palsy, ataxia, and areflexia. While this condition usually is mild and self-limiting, findings may fulfill many of the criteria in the clinical examination for brain death. Unlike brain death, however, it is not associated with irreparable structural damage of the brain or, as is mandatory, does it fulfill a very important prerequisite of brain death, the exclusion of potentially reversible causes of coma.  Treatment of Miller Fisher syndrome is supportive.

Ophtalmopareses is the most frequent ocular sign in Guillain-Barre syndrome and 3rd nerve abnormalities occur in 10-17% of patients.

Areflexia is noted in nearly all Guillain-Barré Syndrome patients and is due to large diameter muscle spindle afferent axon involvement, Parry 1993. 

MFS presents similar to GBS in a somewhat reverse order. At first the patient may become unresponsive to light, with sluggishly reactive pupils, which can quickly lead to fixed, dilated pupils with progression. The nerve pathways controlling eye muscles may become affected resulting in total ophthalmoplegia (eye paralysis). There may be no verbal response, no motor response, and no occular response. 

 

A patient with GBS who was totally paralysed and developed "fixed dilated pupils" during the course of his illness is reported in the literature and there are many such cases.

 Papilledema secondary to elevated intracranial pressure is present in some cases.

A further variant of GBS, Bickerstaff’s brainstem encephalitis (BBE) is characterized by acute onset of ophthalmoplegia, ataxia, disturbance of consciousness, hyperreflexia or Babinski’s sign (Bickerstaff, 1957; Al-Din et al.,1982).  Large, irregular hyperintense lesions located mainly in the brainstem, especially in the pons, midbrain and medulla are described in the literature.  BBE despite severe initial presentation usually has a good prognosis. MRI plays a critical role in the diagnosis of BBE.

A considerable number of BBE patients have associated axonal Guillain–Barré syndrome, indicative that the two disorders are closely related and form a continuous spectrum.

Encephalitis, an inflammation of the brain parenchyma, presents as diffuse and/or focal neuropsychological dysfunction. From an epidemiologic and pathophysiologic perspective, encephalitis is distinct from meningitis, though on clinical evaluation the 2 often coexist with signs and symptoms of meningeal  inflammation. The etiology of encephalitis is usually infectious, but may be noninfectious, such as the demyelinating process in acute disseminated encephalitis.

 

In a number of the reported cases, meningitis or encephalitis overlaped with flaccid weakness progressing over 3-8 days, with a tendency to be proximal and asymetric.

Laboratory abnormalities have included hyponatremia, including an initial CSF neutrophilic pleocytosis, marked by an elevated neutrophil count.  Normal CSF protein level does not rule out GBS because the CSF protein level remains normal in 10% of patients and because any rise in the CSF protein level may not be observed until 1-2 weeks after the onset of weakness.  Electrodiagnostic studies may show reduced motor amplitudes with normal conduction velocities with active denervation and reduced sensory amplitudes have also been seen.

When clinical or radiological abnormalities are found, the condition may be referred to as Bickerstaff's brainstem encephalopathy (BBE).

 Encephalopathy with peripheral neuropathy may falsely mimic brainstem death.

Acute panautonomic neuropathy is probably the rarest of all the GBS variants.  Diffuse sympathetic, parasympathetic nervous systems are involved. Cardiovascular involvement is common (postural hypotension, tachycardia, hypertension, dysrhythmias).  The acute panautonomic neuropathies appear to comprise an overlaping spectrum of unusual presenting symptoms and/or atypical variants of GBS with a somatic/autonomic involvement.  

The somatic nervous system is the part of the peripheral nervous system associated with the voluntary control of body movements through the action of skeletal muscles, and with reception of external stimuli, which helps keep the body in touch with its surroundings (e.g., touch, hearing, and sight). The system includes all the neurons connected with muscles, skin and sense organs. The somatic nervous system consists of efferent nerves responsible for sending brain signals for muscle contraction.

All variants have in common absent or diminished tendon reflexes, elevated CSF protein concentrations, and electrodiagnostic abnormalities.

Guillain-Barré syndrome is the most common form of acute neuropathy. Also known as acute postinfectious polyradiculoneuropathy (the nerve or nerves may be inflamed, "pinched," or lack blood flow).

Compare postinfectious polyradiculoneuropathy with postinfectious encephalitis.

The signs and symptoms of Guillain Barre Syndrome are almost indistinguishable from that of the West Nile Virus and visa-versa, as both share a propensity  for presenting similarily with muscle weakness and flaccid paralysis. In fact,  GBS and WNV ofter imimc each other.

West Nile virus is a cause of aseptic meningitis that has recently spread across the United States to Canada. Usually, West Nile virus causes a self-limited (gets better on its own, without treatment) meningitis. Infrequently, it causes a more severe illness, which may include encephalitis (inflammation in the actual brain tissue) or paralysis similar to that seen in polio. These severe forms usually occur in elderly people or people with lowered immunity. In this case, the meningitis may mimic the signs and symptoms of hepatic encephalopathy, or hepatic coma.

 Encephalitis is often described as a rare complication of common infections.

Encephalitis simply means inflammation of the brain.  It is usually caused by a viral infection but can also be caused by parasites, bacteria and fungi.  Inflammation of the brain can also result from metabolic disturbances, or be a side effect of some drugs. Nerve cells themselves are not the major target of damage but rather their "electrical insulation coat" (myelin sheath) which results in abnormal brain function. It has recently been recognised that there are other forms of encephalitis that result from attack of the brain by the body’s immune system. Some of these types of autoimmune encephalitis are identified by finding a specific antibody in blood.

 

Most cases of acute flaccid paralysis with a preserved sensorium result from diffuse disorders of the motor unit, such as in axonal polyneuropathy or axonal demyelinating neuropathy. 

 

Since the widespread application of the vaccine preventing paralytic poliomyelitis, the number one cause of acute neuromuscular weakness in the developed world is Guillain-Barre Syndrome (GBS).

Obtundation in GBS: The term refers to a reduction in alertness and arousal in which these patients only appear to be completely unresponsive. Although patients with GBS in the setting of preserved consciousness may be described as obtunded, patients may be fully lucid; ambiguities in deciding whether some individual patients are truly unconscious, in a vegitative state, or simply locked-in (implies fully preserved consciousness) cannot be diagnosed on the basis of a paltry CT.

The locked-in syndrome (pseudocoma) describes patients who are awake and conscious but selectively de-efferented, i.e., have no means of producing speech, limb or facial movements.

GBS may induce a "locked-in" state of 'outer calm inner panic' due to a severely paralyzed motor function that patients are able to recall vividly and unpleasantly. A comparable awake conscious state simulating unresponsiveness may also occur in severe cases of peripheral polyneuropathy as a result of total paralysis of limb, bulbar, and ocular musculature.

The locked-in state (LIS) involves damage to corticospinal and corticobulbar pathways in the basis pontis. GBS causes bilateral profound damage to these pathways with diffuse compromise to peripheral nerves. Nerve conduction study helps differentiate the heterogeneous subtypes of GBS.  

Transient LIS cases have been reported after Guillain Barré polyradiculoneuropathy (Loebet al., 1984; Bakshi et al., 1997; Ragazzoni et al.,2000) and severe postinfectious polyneuropathy (Carroll and Mastaglia, 1979; O’Donnell, 1979).

 

GBS is an uncommon paralysing illness, usually caused by autoimmune inflammation of nerves, usually following a course of infection. Recent infections are closely related to the appearance of GBS and are reported by about two-thirds of people with this condition.

Autoimmune disorders destroying nerve function can rapidly lead to weakness and paralysis. The disorder often manifests itself by a rapid onset of weakness and/or paralysis of the legs, arms, face. and  breathing muscles. Breathing is affected by weakening the muscles of the chest wall and diaphragm; in these cases, mechanical ventilation is required immediately.

A feature common in all GBS variants is a rapidly evolving polyradiculoneuropathy preceded by a triggering event. GBS is primarily a disorder of nerve inflammation involving progressive muscle weakness or paralysis, which often follows a therapeutic regimen. It occurs more freequently  in patients with meningitis, encephalitis, pneumonia, septicemia, severe malaria, bronchiolitis, RSV infection, including a variety of primary and secondary disorders. GBS is often caused by an immune system response to a trigger, such as 'drug-drug' interaction caused by combining drugs. Further, influenza immunization also has been associated with GBS.

GBS can result in muscle weakness, pain, and even temporary paralysis of the facial, chest, and leg muscles. The mechanism of pain is thought to be inflamed nerve roots. Paralysis of the chest muscles can lead to breathing problems. Severity may range from mild weakness to complete tetraplegia with ventilatory failure. Peak deficits are reached by 4 weeks after initial development of symptoms. Recovery usually begins 2-4 weeks after progression ceases.

GBS may be triggered after or during the course of treatment for a variety of infectious processes, bacterial or viral. In particular, infections of the gastrointestinal (GI) tract or respiratory system are most commonly associated with the condition.  It is an  immune-mediated type of delayed allergic response secondary to certain medications, or an iatrogenic immune mediated neuropathic reaction to contraindicated medications, or both.

Ignorance of the possibility of a reaction is clear evidence of negligence.

 

Guillain-Barré syndrome is a 'post-infectious immune-mediated' disease. The hypothalamus (the part of the brain that works directly with the pituitary gland to produce hormones) is a "target" for 'post-infectious immune-mediated' disease.   The hypothalamus controls thirst and urination, sleep, body temperature, appetite, and blood pressure. 

The symptoms of GBS can mimic those of other neurological diseases, including brainstem death.  

GBS is a form of autoimmune disease with a delayed hypersensitivity reaction. It is a rare manifestation of serum sickness or a transient syndrome resembling serum sickness with loss of appetite, nausea, vomiting, and stomach pain accompanied by weakness (tired feeling), chills, low grade fever and possible evidence of brain involvement, indicated by lethargy and migraine headaches, although one theory of the cause of migraine is a central nervous system (CNS) disorder, or Bickerstaff's brain stem encephalitis.  

Typical pain is occipital or in the back of the head. Alterations of consciousness go with this headache type affecting the brainstem implicated in the maintenance of arousal, but is a worrisome feature of this type of headache called a Bickerstaff migraine.

Other related headache syndromes also seem to involve the brainstem. There is ophthalmoplegic migraine that implicates the oculomotor (IIIrd) nerve with ptosis and double vision that may or may not involve the pupil or sometimes the VIth or abducent nerve.

Meningitis or meningeal infiltrative disorders usually result in third cranial nerve palsy and 3rd cranial nerve palsy is an exceptionally rare manifestation of GBS, expanding the spectrum of clinical signs and neuraxisinvolvement that may be seen in the condition. Although third-nerve palsy occurs in up tp 17% of cases, most resolve without sequelae.

Other features of Bickerstaff migraine go with involvement primarily of the brainstem including clumsiness and gait unsteadiness, ie. "pulling to the right".

Serum sickness is of itself a type of delayed allergic response. Vaccines, broad spectrum antibiotics and "virus in stealth" to help kill cancer cells are themselves an onslaught on the immune system which can cause serum sickness leading to GBS, or "provocation polio", which is a hallmark of GBS. The most serious complications of serum sickness are nerve conditions such as Guillain-Barre syndrome and peripheral neuritis.

CNS pathology is frequent in patients with GBS. It involves axons with secondary myolin impairment, microglial activation and inflammatory infiltration. Myelinated axons are white in appearance, hence the "white matter" of the brain. White matter inflammation causes the brain-blood barrier to become partially ineffective.

Other variants are notable for an axonal pattern of electrodiagnostic findings and axonal pathology with little inflamation.

Differential diagnosis

The possibility of West Nile Virus (WNV) meningoencephalitis should also be entertained in the setting of suspected Guillain-Barré syndrome, as management of the two entities is markedly divergent. With WNV, findings in the brain can mimic demyelinating processes.

Compare West Nile encephalitis

Evidence of West Nile encephalitis virus (polio-like) infection has been documented in most states of the continental United States and Canada within a short period of its first introduction in 1999. Health care providers are mostly aware of the usual presentations of this disease, eg, "aseptic meningitis, encephalitis and Guillain-Barré syndrome", suggesting a  shared mechanism.

West Nile virus transmission occurs mostly during warm weather, when mosquito populations are active.  Peak transmission of the WNV occurs between July and October, but cases have occurred as early as April. Further, numerous cases of WNV infection via transfusion of blood products (from asymptomatic, viremic donors) have been  reported. WNV has been associated with severe cerebral abnormalities, including microcephaly and intracranial calcifications.

West Nile virus encephalitis mimicking central nervous system metastases from small cell lung cancer is reported in the literature.  The American Journal of Medicine , Volume 115 , Issue 7, Pages 594 - 595 A . Jeyakumar

WNV-infected individuals are asymptomatic in 80% of cases. Symptomatic illness develops 2–14 days following contraction; 20% of patients develop West Nile fever, a self-limited flu-like illness characterized by fever, myalgia, headache and gastrointestinal disturbance (25–30%), with an associated maculopapular rash in 25–50% of cases.24 Neuroinvasive disease occurs in less than 1% of cases (1 in 150 infected individuals), following viral penetration of the blood–brain barrier and direct invasion of neurons, particularly those in the brainstem, deep nuclei, and anterior horn of the spinal cord. In mouse models, WNV has been shown to increase blood–brain barrier permeability by inducing a Toll-like-receptor-3 (Tlr3)-dependent inflammatory response.25 The clinical and laboratory criteria for distinguishing neuroinvasive from non-neuroinvasive arthropod-borne viral diseases (including WNV) have recently been updated.7 Neuroinvasive presentations (Box 1) are varied and include aseptic meningitis, meningoencephalitis and AFP syndrome (a poliomyelitis-like illness).5, 26, 27, 28, 29, 30 Brainstem encephalitis, cerebellitis, movement disorders, cranial neuropathies, polyneuropathy/radiculopathy, chorioretinitis and optic neuritis are also recognized WNV neurological presentations.

Disease attributed to WNV presents in one of four clinical fashions: West Nile fever, meningoencephalitis, a flaccid paralysis (polio-like syndrome), and a Parkinson-like syndrome. Immunocompromised hosts appear to be at greatest risk for disease. Diabetes, hypertension and cerebrovascular disease have also been considered as possible risk factors.

Although the exact mechanism of illness is unknown, West Nile virus probably enters the host's bloodstream, multiplies and moves on to the brain, crossing the blood-brain barrier — a barrier that separates the blood from the central nervous system. Once the virus crosses that barrier and infects the brain or its linings, an inflammatory response occurs and symptoms arise.

Disease attributed to WNV presents in one of four clinical fashions: West Nile fever, meningoencephalitis, a flaccid paralysis (polio-like syndrome), and a Parkinson-like syndrome. Elderly immunocompromised hosts appear to be at greatest risk for disease.

Interestingly Dr. de la Rocha had a vested interest in West Nile Virus research, and in fact is a Co-author  on the subject of estimating the "Prevalence of West Nile Virus Infection",  West Nile virus is like the flu.

 

GBS can present with focal neurologic deficits or symptoms similar to Parkinsons disease, polio, and West Nile Virus.

 

The diagnosis of Guillain-Barré syndrome is based on typical clinical features, electrodiagnostic examination, and examination of the cerebrospinal fluid.

Macrophage-associated demyelination confirms the diagnosis of acute inflammatory demyelinating  polyneuropathy (Guillain-Barré syndrome). Demyelination is the act of demyelinating, or the loss of the myelin sheath insulating the nerves, and is the hallmark of some neurodegenerative autoimmune diseases, including multiple sclerosis, acute disseminated encephalomyelitis, transverse myelitis, Alexander's disease, chronic inflammatory demyelinating polyneuropathy,  central pontine myelinosis, and Guillain-Barré Syndrome.

A demyelinating disease is any condition that results in damage to the protective covering (myelin sheath) that surrounds nerves in your brain and spinal cord. When the myelin is damaged, nerve impulses slow or even stop, causing neurological problems.

Demyelinating neuropathies are commonly inflammatory and treatable.

 

Treating GBS

GBS is fairly easy for doctors to identify from a person’s description of his or her symptoms and a neurological examination. They can establish the diagnosis with more certainty through electrical testing of the nerves (electromyogram) and sampling the spinal fluid to see if it shows an increase in the amount of protein. Cases with unusual features may be more difficult to diagnose. Neurologists usually direct the care of people with GBS. If major medical problems arise, or if respiratory failure requires the use of a ventilator, a specialist in intensive care, pulmonary medicine, or anesthesia usually becomes involved as well.

Intravenous immunoglobulin (IVIg) and plasma exchange are often used as treatments in this patient group.  Plasmapheresis removes or dilutes the circulating immune factors implicated in the pathogenesis of GBS.  Treatment used in GBS include anticoagulation, IVIG, plasmapheresis, and high-dose corticosteroids. According to a Cochrane review abstract and plain language summary prepared and maintained by The Cochrane Collaboration, currently published in The Cochrane Database of Systematic Reviews 2007 Issue 2, Fisher syndrome always and Bickerstaff's brain stem encephalitis usually recovers completely.

Several treatments seem to shorten the course of GBS, but they are not cures and they do not seem to influence the disease’s course in all individuals. The first therapy shown to be effective was plasma exchange. This process starts with removing some of the patient’s blood and spinning it in a centrifuge machine in order to separate the plasma from the blood cells. Only the cells are returned to the patient’s body, with the missing plasma replaced by an artificial fluid. In this procedure, a tube must be placed in one of the large veins of the chest or neck to bring enough blood to the centrifuge machine.

Parry, 1993, describes "the best quality supportive care" as the cornerstone for the treatment of Guillain-Barré Syndrome.

The acute presentation of GBS is a neurological emergency.

 

The FACTS

 

Arlene Berry developed "flu-like" symptoms suggestive of gastrointestinal illness within two weeks following radiation therapy, at the end of April of 2000.  She died about about 10 days later, on the 24th of May of 2000. Total time lapse 24 days; mean 3 weeks plus, or just under 4 weeks. 

Guillain-Barré syndrome (GBS), is a post-infectious immune-mediated demyelination of the peripheral nerves,  most often seen 2-4 weeks after a respiratory or gastrointestinal illness.  It is a rare manifestation of serum sickness with a  'delayed hypersensitivity reaction', triggered by catastrophic over-stimmulation of the immune system. Peripheral nerves and spinal roots are the major sites of demyelination, but cranial nerves also may be involved.

The most serious complications of serum sickness are nerve conditions such as GBS and peripheral neuritis.  Guillain-Barré Overlap syndrome is a constellation of atypical GBS variants and related disorders.

 

In December of 1999, Arlene Berry was sent to Timmins & District Hospital in Timmins, Ontario, where she was diagnosed, according to her physician, with "carcinoma of the left main bronchus with residual cancer of the aorta due to a complete collapse of the left lung". 

Her family MD,  Dr. Edward. H Jordan  had been treating her 'assumptively' for what he termed a "suspected bronchitis".  It took another doctor to read her X-ray chart,  and to order more appropriate testing before anything was done.

On or about January 12th of 2000,  Arlene Berry was admitted to the Timmins & District Hospital in Timmins, Ontario,  where she had a left lung pneumonectomy on January 13th of 2000, under the care of Dr. Claudio de la Rocha,  a Cardiovascular and Thoracic Surgeon who immigrated to Canada from Mexico.   

Mexico is a hotbed for amebic infection (amebiasis ), a source of infectious cysts.

 

Some people can be 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 unfamiliar infectious diseases, such as amebiasis (a gastrointestinal disease) and also pose public health risks from a variety of emerging infectious diseases.

The most common signs of amebic infection are alternating diarrhea and constipation (possibly accompanied by blood and excessive mucus) and irregular appetite. Other clinical signs include vomiting, listlessness, weakness, low weight and signs of dehydration (e.g.sunken eyes, thick oral mucus). If the lungs are infected (a condition generally associated with more chronic infections), labored breathing, mouth/nasal discharge and wheezing may also be noted.

An ameboma may simulate an "adenocarcinoma" or another granulomatous process.

Ameboma, the forgotten granuloma? 

In the Canada and the United States, amebiasis is most often found in immigrants from developing countries, such as Dr. de la Rocha.  It also is found in people who have traveled to (or who have come into contact with)  developing countries and in people who live in institutions that have poor sanitary conditions which pose health issues for travelers.

 

Ameba only multiplies rapidly if a person is very run down by an immune deficiency, illness or infection. Only virulent amoeba can lyse polymorphonuclear leukocytes (PMNs).

Ameba can spread hematogeneously from a cutaneous, ocular, or pulmonary lesion to the CNS, where vasculitis may also dominate the clinical picture.

 

Further, Dr. Claudio Alberto de la Rocha was charged with failure to maintain the standard of practice and breaking the law after he euthenised a 68-year-old patient by administering a noxious substance. He was found guilty.

Following surgery,  Arlene Berry was discharged home 5 days later.  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 with mediastinotomy,  as part of her  post-operative  evaluation. 

Following that testing, Arlene confided  "I don't have AIDS, or brain tumors, or anything like that, but I might have a "cyst", or "infection".  A cyst is a suitcase for the infectious material inside.  Some of them  parasites with  simulation of stroke related damage in cultured human nerve cells has been reported.

Arlene was diagnosed by de la Rocha as having "adenocarcinoma". Dr. de la Rocha performed a left lung pneumonectomy on January 13th of 2000;  a follow-up was done April 16th of 2000 -  detecting a "cyst" with an associated infection.

Demyelinating lesions rarely can have a cyst-like appearance. These lesions can present clinically and radiologically as brain tumors (gliomas or metastases) or as multiple cysts mimicking tumors.

Parasitic cysts of any origin may mimic primary or metastatic brain tumor(s).

 

She was then referred to the Northeastern Ontario Regional Cancer Centre situated at the Laurentian Site, Sudbury, Ontario for consideration of radiation therapy, under the care of Dr. Hugh Prichard, a  radiation oncologist.  By the end of  April 2000, Arlene Berry had completed her post-operative course of radiation therapy.  In light of this treatment, her condition was seen to be stable.  She had been scheduled for X-ray follow-up in Sudbury on Tuesday May 30th at 2:30 PM.

Following  radiation, Arlene Berry  remained quite well, until about one week prior to her admission to the  Kirkland and District Hospital on o May 23rd of 2000,  with the exception of  "a suspected UTI", which was never confirmed. 

According to the hospital record Arlene Berry was admitted to the Kirkland and District Hospital on May 23rd of 2000 by Dr. Spiller for "IV fluid and Gravol", evidenced at A-6.  From that record it seems clear that either Dr. Spiller lied, or that he was totally oblivious to the administration of MS Contin (Morphine Sulfate) evidenced at A-12.  According to the same record she was admitted for "vomiting".  Vomiting is not a diagnosis, but rather a symptom of many causes.

According to record she was given more than IV and Gravol. If not Dr. Spiller, who ordered the 30 mg MS Contin on his watch?

 

 

For the two-week period prior to her hospital admission, her headaches, were accompanied by  stomach pain , loss of appetite, nausea and vomiting, weakness, fatigue, and feeling unusually cold. In the last week of her life,  she developed headaches which at times had become increasingly severe.   

Pain syndromes of Guillain-Barré are usually neuropathic due to inflamation, as well as nociceptive in origin. Typically back pain, radiculopathic and musculoskeletal (often ‘straight leg raise’ positive).

A-5 of the record documents the presenting complaint as "headaches, accompanied by severe stomach pain", and  "abdominal pain ongoing for 2 weeks", for which she was prescribed "antibiotics".     

Abdominal or 'stomach pain concurrent with  nausea and vomiting  points to the abdomen' as the source of the problem which should have been a 'red flag' suggesting the possibility of "intestinal obstruction".  Abdominal pain can also be the result of "intestinal ischemia". The hallmark of intestinal ischemia is "abdominal pain".

Headache in GBS is unusual, but has been reported.  Irritated, inflamed or damaged nerves in the brain, spinal cord or body can cause headache with increasing severety, as can ophthalmoplegia associated migraine in the Miller Fisher variant of GBS, as the disorder progresses.

There is also an ophthalmoplegic migraine that implicates the oculomotor (IIIrd) nerve with ptosis and double vision that may or may not involve the pupil or sometimes the VIth or abducent nerve.

MFS: minimal motor weakness, gait ataxia, areflexia (or hyporeflexia), and diplopia (ophthalmoparesis), facial sagging and slurred speech (indicates all cranial nerves, esp. VII, but not I or II)

  GBS may encompass a wide range of adversities. Many secondary complications that follow GBS include deep vein thrombosis, anemia, and mild to moderate migraine attacks in which underlying causes of headache may also include  bowel dysfunction with severity.

 

Other Complications include:

Significant complications of Guillain­Barre syndrome include mechanical ventilatory failure, aspiration pneumonia, sepsis, joint contractures, and deep vein thrombosis. Unexplained autonomic nervous system involvement may cause sinus tachycardia or bradycardia, hypertension, orthostatic hypotension, and loss of bladder and bowel sphincter control.

The features of abdominal migraine is an abrupt on-set of severe abdominal pain followed by an abrupt discontinuation of symptoms. Abdominal migraine is one of the variants of migraine headache, ie. (headache lethargic migraine).  A strong family history of migraine headaches is a common finding.

Migraine headaches happen when blood vessels in your head open too wide or close too tight. The most common triggering agents for migraines are alterations in serotonin metabolism (deficiency), diabetic condition, hormonal imbalances, histamine-induced platelet aggregation (blood platelets sticking together), blood sugar imbalances and certain medications. 

 In women, migraine attacks may also be triggered by hormonal changes during menstruation (periods).

According to the record at OP-53 she was "Here 1 week ago for UTI. Last period on 6th of May". Onset of menstrual period is closely related to onset of migraine headaches, including illness. 

Case reports cited primarily in women having period in which a blood-soaked tampon may provide an excellent breeding ground for the bacteria which causes Toxic Shock Syndrome (TSS), and is a significant cause of urinary tract infections. TSS is a variant of septic shock and bacteremic shock. It presents with a sepsis-like picture. Severe sepsis may mimic TSS.

Sepsis is a frequent complication of GBS.

Sepsis refers to the presence of an infection, plus any two of these four criteria:

Visible symptoms of sepsis include nausea, vomiting and chills in the presence of an infection.

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 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.

Severe sepsis is a condition in which sepsis is accompanied by associated acute dysfunction in one or more of the organs. Septic shock refers to a severe sepsis case in which the cardiovascular system begins to fail, blood pressure drops, and vital organs are deprived of adequate blood supply.

 

The RN  who saw her noted that she had  been "taking morphine"  for pain management, and also that she had recently  "stopped"  taking the morphine,  noting her recent medical history that for "2 weeks"  she had the "flu".  The same record also documents a question mark (?) with respect to possible morphine allergies, seen at A-5. 

 Sudden stoppage of drugs can cause a rebound phenomenon: relapse with or without exacerbation of the basic disease, or exacerbation of the basic disease, or a withdrawal phenomenon: a new clinical syndrome unrelated to the original disease.

Guillain-Barré syndrome (GBS) has become an umbrella term for different disorders representing a collection of clinical syndromes, some of which may overlap each other.

In this instance, withdrawal from opiates may result in a mixed picture of two syndromes: eg., a typical Guillain-Barré  syndrome and a generic withdrawal syndrome,  with signs  and symptoms reminiscent of those observed with use of narcotic analgesiscs.

In fact, there could well be a shared mechanism for each and every disorder underlying illness, resulting in a mixed picture representative of multiple syndromes. 

OP-53  documents a history of Tylenol and Aspirin, including a documented "daughter states takes a lot",  suggests a history of drugs that can break the gastric barrier, and damage the gastric mucosa, ie., NSAID's (non-steroidal anti-inflammatory drugs). Aspirin is the drug classically associated with Reye syndrome.

According to the patient's Rx list, Arlene Berry  had been given sodium  phosphate (used to treat constipation) while under the care of her oncologist, and sodium dosucate prescribed by her family MD, and to the best of my knowledge kept taking them following her discharge home, until her prescription ran out. She had found the prescribed laxitives to be ineffective and so turned to over the counter laxitive and tap water enemas for what appeared be drug opiate induced dysmotility.

 









Enema is contraindicated in patients who present with fulminant disease, because of the danger of precipitating toxic megacolon or perforation of the colon.

 

Coadministration of narcotic analgesics with laxitives may have additive central nervous system (CNS) and gastrointestinal (GI) system effects, and increase the risk of severe constipation or paralytic ileus, including CNS depression.

 Straining to evacuate the bowel may also contribute to increased  intracranial pressure (ICP).

 

Guillain-Barre with unusual autonomic dysfunction at its onset, consisting of constipation and hypertension, followed by adynamic ileus, endocrine abnormalities and flaccid paraparesis with areflexia limited to the lower limbs is also reported in the literature. 

 

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".

The record at A-17 documents  a "0" use of acc muscles; and a "0" use of abd muscles.

 Hypotonia in Guillain-Barré syndrome is common and can be observed with significant weakness. It is characterized by diminished resistance of the abdominal muscles, with diminished tone of the skeletal muscles; most notable for a "soft, non-tender abdomen". The abdominal muscles feel 'soft and doughy'. Also a sign of gastropareses in clinical diabetes, which can rapidly progress to intestinal obstruction.

Gastroparesis  shows a strong female predominance, and menstrual cycles are important; in the week before menses, when progesterone levels are high, nausea and vomiting can be exacerbated. Patients with  Gastroparesis have emesis of undigested food consumed many hours or even days previously. 

Gastroparesis may occur in relation to systemic diseases, such as diabetes mellitus. Diabetics with autonomic neuropathy may also delelop  neurogenic bladder. For some females, a clear pattern may be seen following the menstrual period, especially in patients with a suspected UTI.  

Gastroparesis affects up to 75% of people with diabetes.

According to the record at A-6 she returned to the ED (emergency department) on May 23rd of 2000  "with the very same complaints". On examination, the physician who saw her documented positive bowel sounds with no rebound tenderness.  Paucity or absence of bowel sounds suggests paralytic ileus.

Sometimes audible without a stethoscope, hyperactive bowel sounds reflect increased intestinal motility (peristalsis). They're commonly characterized as rapid, rushing, gurgling waves of sounds. They may stem from life-threatening bowel obstruction, or GI hemorrhage. 

 See Characteristics of bowel sounds.

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

What appears to be a referral at A-6 of the medical record, a chart-copy from the admitting physician (Dr. Spiller), directed to the attention of the family physician Dr. Jordan, documents what I take to be a provisional diagnosis of "vomiting",  while the record at  N-11 documents "vomiting, lung CA".

At the time of her admission to the hospital, Arlene Berry's blood pressure was documented at 115/70 bpm, with a pulse of 79 and regular. with signs of  "mild diffuse weakness",  as occurs in onset widespread neurologic or muscular diseases, evidenced at A-6.  The same record documents that she was having  "difficulty ambulating".  She developed "diffuse weakness" and pain with activity and difficulty ambulating.

The weakness progressed so that she was "pulling to the right" and unable to stand, suggesting a more cephalad (proceeding toward the head) level of infection, prompting an ER evaluation.

A history of increasing or "diffuse muscle weakness" followed by paralysis suggests a typical presentation of Guillain-Barre syndrome, especially if there was a recent illness, or infection.

People with GBS generally notice weakness in their legs, manifesting as "rubbery legs" or legs that tend to buckle, which may cause the patient to pull or fall in one direction or another due to unsteadiness, resulting in difficulty ambulating. Only about 28% of patients with the GBS remain able to walk unaided. Patients with the hyper acute form of the syndrome lose the use of their legs within a day.

The  record at  A-6,   documents a respiratory rate of 18, on admission.  The normal adult respiration rate is 12 to 18 breaths per minute.  It seems clear that the patient had normal respiratory function at tconsist hat time, and the time of this assessment, Arlene Berry  was found to be "alert and oriented", with "NO Focal deficits". 

A set of symptoms may represent a very mild form of GBS. The clinical features of GBS range from asymptomatic to life threatening. In the initial stages, the patient is likely to have few if any symptoms (Hughes, 1995).   In contrast to the  mild forms, at the other extreme a GBS patient may become totally paralyzed and fraught with complications.

Within a few hours of her admission, Arlene Berry developed a rapid progression of muscle weakness, apnea, and laboured breathing Cheyne Stokes pattern, a prominant finding in bilateral diencephalic insult.

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.  Snoring, sleep apnea, cheyne-stokes breathing and gasping for breath are all part of the same problem.

Look at the shape of the neck. Adults and older adolescents having short thick necks are at greater risk of developing obstructive sleep apnoea. Aspiration and respiratory failure are major concerns. Moreover, respiratory failure is one of the most disastrous disturbances of neuromusclar diseases such as Guillain Barre Syndrome and poliomyelitis. In fact, the major part of treatment for these type of disorders consists of measures that assist respiration (mechanical ventilators).

According to the outpatient record at OP-54, the patient's recent head CT scan showed "NO METASTASIS", and her mediastinoscopy, a surgical procedure to examine the mediastinum inside of the upper chest between and in front of the lungs, were found to be "NEGATIVE".  From that record it seems clear that NO clinically detectable metastasis were found. 

The Health Management Record at A-21 of the record documents her sensory cognitive perceptual pattern as "sedated". Increased sedation is also a serious side effect of many pharma agents, including electrolyte derangements which can mimic sedative intoxication.

GBS may herald an onset of sleepiness in a subset of patients, presenting with mild to moderate fatigue, to "sleep drunkenness" in which the patient often appears to be "sedated" due to extreme somnolence.  In frail patients, as the respiratory rate decreases, the patient becomes increasingly sedated. 

What the family had found to be peculiar however, was a dramatic voice change following the mediastinal procedures, suggesting  a "partial vocal fold paralysis" thought to have been procedure related.  Although she began to regain her voice in the weeks that followed, the voice remained somewhat "whispery" for the memainder of her days.

The record at  A-23 documents a "slurred" speech as evidenced by a checkmark  in the upper left corner. Speech may be unintelligible, "slurred" or whispery with GBS, as the various muscles required to form speech are weakened.

Vocal cord paralysis is a prominent finding in patients with GBS and there can be a slight to dramatic voice change as the vocal chords become affected.

 

GBS is associated with prominant involvement of the speech and swallowing muscles and suppression of the gag reflex due to swallowing difficulty, with alterations in speech patterns or dysarthria attributed to muscle paralysis.

 

The emergency record from the hospital dated May 22nd of 2000, seen at  OP-54  documents a recent history of hematuria (blood in urine) for "three days" and a prescription for Ciprofloxacin (Cipro), for treatment of urinary-tract infection.

An infection of the urinary tract is considered complicated if there is simultaneous evidence of a metabolic disease, functional/anatomical abnormality of the urinary tract, or an infection of the urinary tract, especially with "resistant pathogens".

The healthcare provider who saw her made a diagnosis of "UTI". The belated test result however, what I assume to have been a urology test, or a blood culture test, evidenced at  OP-55 of the Outpatient Record, later returned a finding of "NO Growth". 

 

A negative urine test can also suggest the presence of unusual bacteria or viruses causing symptoms of UTI.

 

The  record at  OP-54  documents "SEPTRA DS GIVEN BEFORE & CIPRO GIVEN AFTER".  The same healthcare provider (whose signature is illegible) also made a notation with respect to the "flu" which was then directed to the attention of the patient's "family MD", namely, Dr. Jordan.  Cipro is an broad-spectrum antibiotic indicated in the treatment of a variety of infections, including the flu.

GBS is an iatrogenic disorder.

 It is  well documented that Cipro causes drug-induced serum sickness, which can rapidly progress to Guillain-Barré syndrome.

Central nervous system complications of many pharma-agents include aseptic meningitis and Guillain-Barré syndrome.

 

Meningitis means inflammation of the membranes covering the brain and spinal cord. When the protecting barriers of the brain, including the skull, meninges, and blood-brain barrier are broached by a pathogen, meningitis can result. Predisposing factors include pre-existing diabetes mellitus, immuno-suppression, otitis media, pneumonia, sinusitis, and alcohol abuse. Meningeal inflammation and irritation elicit a protective reflex to prevent stretching of the inflamed and hypersensitive nerve roots, which is usually but not always detectable clinically as neck stiffness, or meningeal signs. Meningeal irritation due to inflammation also may cause headache and cranial nerve palsies.

Active demyelination is accompanied by transient breakdown of the blood-brain barrier.

 

Aseptic meningitis is one of the most common infections of the meninges. Although it looks like bacterial meningitis, bacteria do not grow in cultures of the cerebrospinal fluid (fluid around the brain and spinal cord). Many different things can cause aseptic meningitis including viruses, fungi, tuberculosis, some medications, and infections near the brain or spinal cord, such as epidural abscesses.

When cerebral edema and elevated intracranial pressure occur, alterations in mental status, headache, vomiting, seizures, and cranial nerve palsies may ensue. Bacterial and aseptic meningitis cannot be distinguished by clinical characteristics alone. Many patients who have aseptic meningitis can be cared for on an outpatient basis, but those who have profound headache, nausea, vomiting, or CSF pleocytosis with a polymorphonuclear leukocyte predominance should be admitted for observation with antibiotic coverage for bacterial meningitis. Encephalitis may develop in some patients.

Drug-induced aseptic meningitis is an uncommon and mysterious adverse reaction to some commonly used medications. This condition can mimic the signs and symptoms of a true infectious meningitis.

 

The incidence of drug-induced meningitis (DIAM) is unknown. Many antimicrobials, such as  ciprofloxacin,  amoxicillin, and penicillin are causes of aseptic meningitis.  DIAM is a complication in which numerous other drugs, namely nonsteroidal anti-inflammatory drugs (NSAIDs), also have been associated.

Classic signs and symptoms of meningitis generally develop within 24 hours of drug ingestion, although it may take days. NSAIDs still account for most cases, although similar reactions to other drugs have been described in the literature involving patients of all ages, with or without pre-existing conditions.

Bactrim/Septra is also the antibiotic most frequently associated with drug-induced aseptic meningitis.

The clinical presentation does not help in differentiating Drug-Induced Aseptic Meningitis (DIAM) from infectious meningitis. The CSF profile (ie, neutrophilic pleocytosis) does not allow DIAM to be distinguished from infectious meningitis. Systemic lupus erythematosus is the single most frequent underlying condition associated with DIAM. Recurrent DIAM is well known; females usually predominate, and the frequency varies with the different underlying conditions. Signs and symptoms generally develop within 24 hours of drug ingestion, although it may sometimes take days.  Repeat exposures to the drug, however, will always demonstrate a quicker onset of symptoms, usually within hours. The patient often exhibits the classic symptoms of meningitis, including headaches, fevers, neck stiffness, mental status changes, malaise, nausea, vomiting, chills, generalized arthralgias, and myalgias.

Characteristics of a hypersensitivity reaction may also be present, such as skin rash, pruritis, conjunctivitis, facial edema, photophobia, or papilledema.

 

Cross-reactions between penicillin and sulfa-drugs are  common triggers of drug-induced GBS serum sickness, and fixed drug eruptions. Cipro and Septra DS have been implicated high on the order of major offenders in drug-induced GBS.

Compare: Serum sickness-like syndrome, generalized allergic reactions, and generalized skin eruptions.

N-9 of the nurses' notes documents a precaution for a "resistant bacteria" , as evidenced by a check mark  in the upper right hand corner of that document, under the subheading for "INFECTION CONTROL PRECAUTIONS", which requires implementation of strict infection control policy. The same precaution is also noted in the upper right hand corner of the record at A-21. The details with respect to the offending organism were omitted from the record, withholding that information from the patient's family.

According to her Rx List, Arlene Berry had also been given Amoxicillin for infection. Amoxicillan belongs to a class of penicillin-like drugs, side effects of which include severe nausea and vomiting, including abdominal pain.

Certain combinations of medications, such as penicillin and sulfa-based antibiotics can cause the body's immune system to react by overstimulation. 

The record at OP-54 dated May 22nd of 2000 documents a "haggard appearance" including "large blood trace leukocytes", what I take to mean leukocyte estrace, marked by an unusually high number of white blood cells (WBC's). When put on a fast, or a restricted diet, causing a steady reduction, in the course of three or four weeks the patients will begin to show a haggard appearance.

 In people with GBS the characteristic appearance of a "haggard" or "mournful" face and drooping eyelids is caused by facial muscle paralysis.

 

Leukostasis results from sludging of high numbers of leukocytes in small vessels, particularly the brain, lungs, and kidneys.

Patients with Guillain-Barré syndrome often appear to be nauseated and in a state of total exhaustion, marked by a "haggard appearance". Involvement of facial, oropharyngeal, and ocular muscles results in facial droop, dysphagia and dysarthria.

 

Cases of Guillain-Barre syndrome can have pleocytosis, or CSF granulocytes. 

Granulocytes are cancer killing cells destroying tumors, cancer-cell turns black as it dies.

"Granuloma" formation is a hallmark of chronic bacterial infection. CBC shows leukocytosis and a shift to immature forms early in the illness.  Leukostasis also results from sludging of high numbers of leukocytes in small vessels, particularly the brain. 

 If left untreated, GBS,  can rapidly lead to respiratory distress syndrome, sepsis, pneumonia, pulmonary emboli, cardiac arrest and death may occur with impaired blood flow as a result of blood clots.

 

  Flag: Counts that are above or below the reference range are recorded in the flag column, and marked with an L for 'low' or H for 'high' ought to have prompted medical attention or intervention, but did NOT.

 

A-19 of the record documents an elevated  WBC Count  of 22.4 H.  The presence of an elevated WBC count is called Leukocytosis. White cell count is actually 22,400.  A normal WBC is 5,000 to 10,000.  Normal Adult Range: 3.8-10.8 thous/mcl
Optimal Adult Reading: 7.3    Compare : Lab Values  

 

WBC = Leukocytes

WBC leukocytes are the body's primary defense against bacterial infection and also reflect the degree of physiologic stress.   WBC's are also elevated with dehydration, and hyperviscosity secondary to dehydration. 

If the total WBC is high due to a rise in neutrophils and eosinophils, then an allergic, or parasitic process is most likely. An increase in the WBC count (leukocytosis) is also a typical response to noxious stimuli.

 

Miller Fisher-Guillain-Barré overlap syndrome is a postinfectious allergic reaction  involving both peripheral nerves in the cranium and neuraxis in the spinocerebellar tract. It is an immune-mediated type of delayed allergic response secondary to certain medications which can rapidly progress to clinical state "resembling brain death".

The record at A-19 documents a Neutrophil count of 92.0 H with an absolute neuts of 20.0 H.

Neutrophils, are also known as "segs", "PMNs" or "polys" (polymorphonuclears). CSF in bacterial meningitis is typically dominated by the presence of PMNs.  PMN’s generally predominate in bacterial infections. "The presence of polymorphonuclear granulocytes does not rule out the diagnosis of Guillain-Barré syndrome". Eur J Neurol 10(5): 479-86.

Neutrophilia (or neutrophil leukocytosis) is a condition where a person has a high number of neutrophil  granulocytes in their blood. Neutrophilia may be due to a number of acute and chronic causes such as  infection, inflammation, emotional stimuli, drugs, metabolic hormonal, and endocrine disturbances, including  hematologic abnormalities. 

Wegener's granulomatosis, granulomatous cerebral amebiasis, vasculitis, and heart attack are high on the order of Neutrophilia.

Leukocytosis, especially neutrophilia, indicates systemic infection and is rare in the absence of bacterial "superinfection". 

Superinfection, also called "superbugs" are bacteria,  viruses or mixed infection which are resistant to antibiotics.

Filthy hospitals and healthcare professionals breed superbugs!

 

 Hypertension, tachycardia, cardiac arrhythmias, and hyperglycemia are examples of systemic effects.

Hyperglycemia as a manifestation of the stress response is most evident after an ICU admission and may resolve as the underlying catabolic illness.

The record at A-19 documents a Lymphocyte count of 2.0 L (low) suggestive of lymphocytopenia in which lymphocytes (T-cells) are reduced with nutritional deficiency, infection, and ascites due to "fluid build-up in the abdomen" , and/or an exhausted immune system.  If bacterial infection is present in ascites this may suggest spontaneous bacterial peritonitis in which abdominal pain is a prominent finding. If peritonitis is not treated promptly and effectively multisystem organ failure occurs rapidly.

GBS - Typical profile: elevated protein (may ttake 1-2 wks. to develop) with normal to mild increase (<10) lymphocytes (albumino-cytologic dissociation).

 The presentation of abdominal abscess is similar to that of peritonitis, but the symptoms are generally milder.

T-cells (lymphocytes), which are mediators of immune function are also involves in the pathogenesis of most or perhaps all forms of Guillain-Barré syndrome. T-cell sensitization causes loss of myelin which disrupts nerve impulses resulting in loss of neurotransmission to the periphery. T cells are directed against myelin proteins P2, P0, or PMP22. These activated T cells release cytokines and activate macrophages that invade the myelin sheaths and cause demyelination.

Symptoms generally coincide pathologically with various patterns of lymphocytic infiltration and macrophage-mediated demyelination, depending on the subtype in question.

Molecular mimicry occurs when an invading pathogen is structurally similar to host cells in order to escape immune detection, which results in the immune system confusing the pathogen with 'self' cells.  When the host produces an immune response to such an invading pathogen, this response inadvertently begins attacking host cells using these same T-cells and antibodies primed by the initial infection with the mimicking pathogen.

Demyelination is the term used for a loss of myelin, a substance in the white matter that insulates nerve endings.  Symptoms generally coincide pathologically with various patterns of lymphocytic infiltration and macrophage-mediated demyelination. Inflammatory infiltration, especially a mixture of lymphocytes and macrophages, favors the diagnosis of demyelination plaque. In such cases the lymphocytes will be predominantly T cells.

 Demyelinating polyradiculoneuropathy can also resemble brain death.

The flaccid phase in GBS may be overthrown by an inadvertent generation of mutant T-cell receptors that are anti-self, marked by an allergic white blood cell picture, or AIDS-like super-immune response, sending white blood cells (called T cells) rampaging through the body destroying its own tissues. 

It is worth noting that, because different people have different immune systems, one person may be pre-disposed to developing GBS, whereas another may not.

GBS can also occur in patients with severe T-cell suppression (T-cells literally become worn out) as a consequence of incomplete recovery following infectious or chemotherapeutic agents, especially radiation which preferentially suppress T-lymphocyte responses.  Thus lymphocytopenia and incomplete recovery are consistent with immunocompromise in patients with GBS.  This form of  lymphocytopenia  is often confused with the disease of the same name  that results in immuno-deficiency. 

Chronic anxiety, stress, depression and panic, have all been shown to compromise health, damage immune function, and result in symptoms almost or identical to AIDS, often resulting in questionable diagnosis. Profound fatigue is associated with panic disorder. Cognitive processes commonly trigger affective responses. Panic, fear, and anxiety are also common affective components of dyspnea.  Anxiety, stress, depression and panic are also prominant findings in GBS.

A-19 documents a Red Blood Cell (RBC) Count of 4.30 (3.80 - 5.80 is normal), but the HCT (Hematocrit) is very low, with a reduction suggestive of anemia.  Anemia is also a prominent cause of dyspnea when the hemoglobin concentration falls below 8-10 g/dl.

The same record seen at A-19 documents an HCT count of only 0.361 L (low):  HCT  is the measurement of the percentage of red blood cells (RBC's) in whole blood. The hematocrit (HCT) is another way of measuring the amount of hemoglobin (Hb), and in this case it is very low.  Thus anemia  is present when HCT is < 37%  in women. 

From the record nothing was done to  transfuse blood to hematocrit (HCT) of 30 or greater.

Most common reasons for a falling HCT include blood loss (ie. bleeding colon), nutrition deficiency, and kidney failure.  Other reasons for a low HCT include dehydration, iatrogenic fluid overload, or vasoconstriction following acute blood loss. Other reasons include exertional fatigue, such as seen  in patients with chronic heart failure, and is usually attributed to skeletal muscle underperfusion. Exertional fatigue, sleep loss, and negative energy balance may result in heart failure.  Moreover, post-exertional fatigue and flu-like symptoms are predictive of lowered cardiac output, a hallmark of CFS.  In this case, due to skeletal muscle dysfunction (underperfusion) in the patient.

A-19   also documents a Hemoglobin with a Count of 120, (reference  120-160).  Hemoglobin carries oxygen supply to vital organs. Normal Values:  Female: 12.1 to 15.1 gm/dl. Hemoglobin (Hb) is the main component of red blood cells; a protein that carries oxygen from the lungs to the body's tissues, and carbon dioxide from the tissues to the lungs to be exhaled. As the hemoglobin declines further, dyspnea becomes more pronounced.

 Dehydration can temporarily increase hemoglobin levels giving rise to a false test. Signs for abnormally low hemoglobin levels are fatigue, fainting, pallor (loss of normal skin color), and shortness of breath, and is confirmed by the RDW, which is markedly elevated. When there are insufficient RBC's (red blood cells), oxygen delivery is compromised.

A-19 documents an  RDW (red blood cell/raw distribution width) of 18.4 H (high):  RDW's principal function is to transport oxygen to the blood and becomes "elevated with oxygen deprivation" and is also increased with blood loss, iron deficiency,  and anemic hemoglobinopathy.  Normal RDW  for an adult female is 12-16 g/dL.

Facts suggest inadequate oxygenation despite the fact that oxygen levels were returned to normal by compensatory mechanisms, marked by a clinically evident inability to adequately ventilate or oxygenate the patient.

 A-19  documents an Absolute Mono's of 0.60 (normal 1.0 - 4.5).  The Absolute monocyte count is age dependent; Count rarely exceeds >1.0 x 109/L.   The monocytes are a type of phagocyte which mature into "macrophages"; they are important germ eating cells. The majority of patients with Guillain-Barré syndrome will have 10 or fewer monocytes. Nearly 40% of GBS patients are seropositive for Campylobacter jejuni. Lymphocytic infiltration and macrophage-mediated demyelination of the peripheral nerves are present. Symptoms generally resolve with remyelination.

 

Patients with a low monocyte count have a higher risk of getting sick from an infection, particularly those caused by bacteria.  In cancer, or leukemia,  the monocytes become elevated. In this case the monocyte count is well below the normal range.

A-20 documents an O2SAT (oxygen saturation)- arterial oxygen saturation (SaO2)  of 98.9 H, with with a NORMAL reference and an evident run time of 1720 hours, notably several hours after the patient's alleged time of death, following her transfer out to Sudbury on May 24th of 2000.

The same record documents an Arterial  Ph of 7.437.  Hydrogen ion concentration expressed as pH "Power of Hydrogen".  A Normal pH is 7.35 - 7.45. The pH is a parameter expressing the acidity of a solution. Neutral pH is 7. For example, the pH of blood is normally 7.4 and that of muscle is 7.0. pH under 7 is acid; pH over 7 is basic or alkaline.

and a PCO2 of 37.0.  Compensation has occurred when pH has returned to normal range.  Compensation is not always total. It may be partial in which case the pH will remain slightly decreased or slightly increased. The time of that assessment is documented at 0400 hours.

A-18  of the medical record documents an "inferior ischemia", a sign of reduced oxygen supply to vital organs due to reduced or poor blood flow to the heart.  An "inferior ischemia" is the hallmark of "impaired organ perfusion", as it implies that, unless corrected,  there may not be enough oxygen in the blood to sustain vital organs. 

The same record at A-18  documents "Sinus Tachycardia". Sinus tachycardia occurs when the sinus rhythm is faster than 100 beats per minute. The rhythm is similar to normal sinus rhythm with the exception that the RR interval is shorter, less than 0.6 seconds. P waves are present and regular and each P-wave is followed by a QRS complex in a ratio of 1:1. At very rapid rates, the P-waves might become superimposed on the preceding T waves such that the P waves are obscured by T waves.

Sinus tachycardia, (>90/min), is seen in over 35% of patients with Guillain-Barré Syndrome, and over 30% suffer from hypertension (Parry, 1993).  Sinus tachycardia results from increased automaticity of the SA node, usually due to increased sympathetic stimulation of the heart,  or cardiac toxicity.

 

Demyelination in reperfusion injury can be caused by a direct invasion of macrophages.  Reactive oxygen metabolites and inflammatory leukocytes also play a major role in the development of reperfusion nerve injury.

 

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". 

OP-53  documents a history of bowel movements when voiding evidenced by  "bloody BM's (bloody, black, or tarry stools) x 4 days".   The same record documents  "pale-looking and lethargic".  Pale skin suggests decreased blood supply to the skin.  Lethargy and drowsiness are often associated with moderate to severe dehydration, including congestive heart failure.  Lethargy may also be caused by the toxic effects of waste products on brain function.

Early symptoms of impending diabetic coma include polyuria, nausea, vomiting and abdominal pain, with lethargy and somnolence.

GBS  impacts the muscles that control the bladder and colon, as a consequence of autonomic dysfunction, caused by damage to nerves that regulate blood pressure, heart rate (tachycardia), bowel and bladder emptying, digestion, and other body functions. Nerve signals can't pass to muscles.

The autonomic nervous system is responsible for the involuntary actions that regulate our heart, gastrointestinal, urinary, muscles, and bowel functions as well as our metabolic and endocrine systems.

Diabetes is the most common endocrine disorder.

 

Acute metabolic derangement and endocrine abnormalities can mimic brain death.

 

Dysautonomia, often causing profound swings in blood pressure (hypotension alternating with hypertension), are often conspicuous in patients with Guillain-Barré. There is even a panic factor marked by sudden onset of intense apprehension, fear, terror, or impending doom with awareness.

 In GBS, dysautonomia is usually acute and reversible.

Severe forms of GBS may result in urinary or fecal incontinence.

Constipation is often a problem in the GBS patient due to the reduced activity of the intestines, change of diet, weakened stomach muscles that resist efforts by the patient to express the intestinal content. Bowel and bladder dysfunction with intestinal muscle paralysis; constipation, obstipation and megacolon is a consequence of defect in the nerve supply of the colon.  A history of grossly bloody stools may also be observed with forcefully unsucessful attempts to evacuate the stool; fecal leukocytes are usually present.

Bloody stools may signify bleeding stomach, diverticular bleeding, or intestinal infection.

Certain medications can inhibit gastrointestinal motility (physically paralyze the intestines) which can exascerbate gastrointestinal problems. Controlled studies have shown that patients with GBS had used antimotility drugs and penicillins more often.

C difficile colitis can develop during or up to 8 weeks after taking antibiotics - is an increasingly aggressive iatrogenic disease.

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 our presence, at which time a cool cloth was provided by the nurses, as evidenced by the record at N-6. 

The same record documents upwards of "100cc yellowish fluid", what is frank 'bile', or "bilious vomit". The time of that assessement was documented at 1915 hours on May 23, 2000, following Arlene Berry's admission to the Kirkland and District Hospital. The same record documents that the patient had stated she was "very tired", whereupon she was then assisted to bed, as evidenced at N-6.

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

The word  "bilious" comes from the word cholera.  The word cholera is Latin for bilious disease and has come to indicate a severe intestinal infection.

 Abnormalities in the respiratory system leads to excessive sleepiness and sensitivity to sedation.

 

 

  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.

 

Fast onset of fatigue in which patients often complain of being "very tired" is a common symptom in patients with Guillain-Barré Syndrome and can be one of the most disabling symptoms.  

Arlene Berry also complained of being "cold"  and so the nurses provided her with extra blankets, is evidenced at N-6.  Her very last words were that she was "feeling a little better", also evidenced by that record.

Feeling unusually "cold" with chilly feelings is a common finding in many subjects with Guillain-Barré Syndrome. 

 Core Body Temp >37.0 C

 A-26 documents a body temperature above 37.0 C at (TIME) According to the record the documented temperature is slightly <38.0 C at approximately 37.8 C, indicative of a very low grade fever. 

Pathogenic bacteria grow best at human body temperature 37ºC.

 

GBS is marked by general malaise, loss of appetite, nausea, vomiting and stomach pain, accompanied by weakness, tired feeling, chills, and sometimes a low-grade fever may be noted, but fever is usually absent and the patient is considered afebrile.

N-5 of the Nurses' Notes documents  "Sudden large queery bloody emesis, reddish brown liquid" at 0255 hours, on May 24th of 2000.

When everything in the intestine slows down, everything in it backs up.

N-3 documents an "Suctioned orally thick brownish secretions" at 0320 hours (in the small hours of the morning), suggestive of a more significant backup of intestinal material, i.e., vomiting of fecal matter due to obstruction of the bowel, evidenced by family present as "a large chocolate coloured (gross appearance), odorless, pasty material, looking pretty much like feces".

If you are unable to open your bowels due to an obstruction somewhere, then your feces cannot exit your body via the normal route and you can get nauseated and start to vomit fecal matter. This condition requires urgent medical attention and probably surgery.

Bulbar weakness and difficulty handling secretions and maintaining an airway may be observed in the GBS patient. Suctioning infers that the patient's airway has become obstructed with secretions or debris.

The same record documents  "suctioned down ET tube several times for small amount of brownish mucous" (a reddish brown liquid, suggestive of old blood or admixture of blood and gastric content) at 0330 hours,  while  A-17   documents "being suctioned for moderate amounts of coffee-ground emesis by RN" at 0330 hours on May 24th.

The record at A-5 documents a blood pressure of 115/75 at 17:05 hours on May 23rd that by 18:45 hours had dropped to 100/50 bpm.

Marked  blood pressure lability with alterations between hypertension and hypotension following paresis suggests an atypical course of GBS. 

 

The record at A-20 documents a Glucose of 13.2 H mmol/L): >236 mg/dl. (the normal range is 4.1 - 7.8).  High blood sugar usually comes on slowly. To convert mmol/l of glucose to mg/dl, multiply by 18. (13.2 x 18 = 237.6).  Plasma glucose >120 mg/dl in the absence of diabetes = clinical sign of sepsis.  

Glucose levels above 11.1 mmol/l (200 mg/dl) at 2 hours confirms a diagnosis of diabetes. Symptoms of severe high blood sugar include drowsiness and difficulty waking up.

 

The blood sugar level has to get above about 180-200 mg/dl for sugar to "spill" into the urine, leading to excesive urination production- below that level, the sugar is reabsorbed after being filtered by the kidneys. So, it’s easy to tell if a person’s excessive thirst and/or urination is caused by diabetes mellitus- the urine will show sugar and the blood sugar level will be elevated.

 

There are many reasons for diabetes, the most common being infection, whether bacterial or viral. The main tissues that can become affected by diabetes are the nerves, kidneys, heart and blood vessels and the eyes.  Higher-than-normal glucose levels may also be caused by: severe stress, heart attack, or stroke.

 

When diabetes is uncontrolled with high blood sugar, the body runs out of water resulting in dehydration with increased concentration of blood leaving the victim prone to blood clots. Concentrated blood is sludging of the blood.

Undiagnosed diabetes often is associated with hyperosmolar hyperglycemic state because of failure to recognize early symptoms of the disease. Myocardial infarction, cerebrovascular accident, pulmonary embolus, and mesenteric thrombosis have been identified as causes of hyperosmolar hyperglycemic state.

The majority of patients with hyperglycemic emergencies present with leukocytosis proportional to blood ketone body concentration. Serum sodium concentration is usually decreased because of the osmotic flux of water from the intracellular to the extracellular space in the presence of hyperglycemia, and less commonly, serum sodium concentration may be falsely lowered by severe hypertriglyceridemia.

 Cerebral edema may result secondary to overly rapid hydration (especially with hypotonic fluids).

Elevated levels of blood glucose (hyperglycemia) lead to many problems.  Hyperglycemia  causes immunosupression leading to infection. Further, cerebral edema can also occur unpredictably in this patient group (especially with hypotonic fluids) from overly rapid electrolyte correction.

Hyperglycemia results from metabolic alterations in glucose metabolism, and is most common in patients with acute illness. Hyperglycemia and hypokalemia were both present on presentation, but  the ED physician, Dr. Mark Spiller neglected to do inherrent bloodwork in a timely manner.  In fact, Dr. Spiller failed in his duty of care to consider  AUTOIMMUNE disorder(s) as a cause for concern.

If your blood sugar levels remain high and you become dehydrated, you are at risk of getting a life-threatening condition called hyperosmolar state, or diabetic ketoacidosis. These are both medical emergencies.

The majority of patients with hyperglycemic emergencies present with leukocytosis proportional to blood ketone body concentration. Serum sodium concentration is usually decreased because of the osmotic flux of water from the intracellular to the extracellular space in the presence of hyperglycemia, and less commonly, serum sodium concentration may be falsely lowered by severe hypertriglyceridemia.

May be alert, lethargic or have a decreased level of consciousness if hyperosmolar.

Hyperglycemia results from a variety of factors, such as the stress response to clinical insult. The major consequences of hyperglycemia are a hyperosmolar state leading to dehydration and a shift in electrolytes from intracellular to extracellular fluids, osmotic diuresis with a subsequent loss of water and electrolytes.

Some patients, particularly those with an untreated underlying process such as infection or ongoing injury, may demonstrate persistent metabolic disregulation and continued hyperglycemia (McCowen et al., 2001).

Diabetes mellitus is characterized by elevated glucose in the plasma and episodic ketoacidosis.

 The hallmark of hyperosmolar hyperglycemic state is profound dehydration, marked hyperglycemia, and often some degree of neurologic impairment with mild or no ketosis. Patients typically present with weakness. Eventually, patients develop neurologic symptoms of lethargy, confusion, hemiparesis (often misdiagnosed as cerebrovascular accident), seizures, or coma.

Hyperglycemia and hyperosmolarity lead to osmotic diuresis and an osmotic shift of fluid to the intravascular space, resulting in further intracellular dehydration.

Hyperosmolar hyperglycemic state (HHS) is a life-threatening emergency caused by high blood sugar (hyperglycemia). It causes severe dehydration and the blood becomes very thick giving rise to blood clot formation.

 

Hyperglycemia itself is a risk factor for soft-tissue infections, ie. brain abscess.

Patients with diabetes may be more prone to infections of the bladder, skin, and vaginal areas, especially in the setting of hyperglycemia. The mechanism is thought to be inhibition of phagocytosis and leukocyte mobilization by hyperglycemia.

 

Hyperglycemia in critically ill patients has been described as a "toxic metabolic milieu" which if left untreated, slowly and insidiously results in catastrophic decline.

The majority of patients with hyperglycemic emergencies present with leukocytosis proportional to blood ketone body concentration. Serum sodium concentration is usually decreased because of the osmotic flux of water from the intracellular to the extracellular space in the presence of hyperglycemia, and less commonly, serum sodium concentration may be falsely lowered by severe hypertriglyceridemia

 

A-20  documents a Sodium level of 144 (137 - 145) mmo1/L. Hyperglycemia can lower the serum sodium concentration by 1.6 mEq/L for each 100 mg/dl, also giving rise to a false test. 

A-20  also documents a serum potassium level of 3.4 L at 0400 hours on May 24th of 2000. Low potassium is defined as a potassium level below 3.5 mEq/L.  Failure to replete potassium in patients who have a total body potassium deficit but an initially normal serum potassium level is a medico-legal pitfall.

Even small changes in the potassium that is present outside the cells can have severe effects on the heart, nerves, and muscles.

 

Hypokalaemic periodic paralysis has a predilection for thyrotoxicity in some patients. It is associated with a low potassium concentration and a normal creatine kinase level.  Further, people who are predisposed to panic and anxiety attacks are also more prone to sleep paralysis (certain diseases causing episodic muscle weakness may result in drop attacks (eg. catalepsy, sleep paralysis).

 

A-20  of the hospital record documents a Creatine Kinase (CK) level of  only 40  units per liter (U/L) at O400 hours.   In females,  total Creatine Kinase  should be 10-79 units per liter (U/L). CK is the  most sensitive enzyme and in the presence of most diseases, levels can be elevated as much as 50 to 100 times the reference level. 

 

Creatine kinase (CK or CPK) is an enzyme or type of protein found in muscle and brain that leaks out and is released into the bloodstream when muscle is damaged.  In normal conditions, there is very little creatine kinase circulating in the blood of the average, healthy human being. Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients.  Even in paraneoplastic disorders the serum CK level typically is elevated  8-100 times normal. 

 

 GBS initially does not usually produce evidence of muscle inflammation or waisting such as elevation of Creatine Kinase (CK) concentration.  Guillain-Barré syndrome is a disorder caused by "nerve" inflammation (not muscle inflamation), involving progressive muscle weakness or paralysis.

 

Persons with GBS or clinically similar disorders typically have normal or low CK levels at onset of the disease, unless tissue damage in the brain or elsewhere has already occurred.

To illustrate, a low/normal CK at the time of a patient's admission would argue favourably against a diagnosis of structural brain damage, or active metastatic cancer, and most favourably for a diagnosis of GBS.

 

Skeletal muscle atrophy is a common comorbidity of cancer. Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients and the progressive depletion of skeletal muscle is a hallmark of many types of advanced cancer. 

A clinical feature of demyelination is muscle weakness without muscle atrophy. Persons with Muscular Dystrophy, Guillain-Barré Syndrome and other neuromuscular disorders have low creatine kinase levels.

Lyme disease may also cause weakness secondary to peripheral neuropathy but it too does not produce evidence of muscle inflammation such as elevation of the CK. 

Creatine Kinase (CK) should typically not be elevated in GBS and if it is, another cause (or underlying disorder) should be suspected.  

The highest creatine kinase activities are found in skeletal muscle, myocardium and brain tissue. Significantly increased creatine kinase levels may support a hypothesis of brain death;  normal CK levels do NOT.

 

 

EVIDENCE OF SUBSTANDARD CARE

 

N-10 of the Nurses' Notes document the patient's level of care as "routine", which showed little or NO concern for patient safety. Further, NO close patient monitoring or toxicological screening was done, marked by a complete absence of nursing care plan, as  evidenced at A-21  of the medical record.  In fact,  NO inherent bloodwork was done in a timely manner. NO protocals were ever followed or implemented, in this case.

Sudden and unexpected deaths have occured in hospitalized patients.

Causes of death include untreated or inadequately treated adult respiratory distress syndrome, sepsis, pneumonia, pulmonary emboli, and cardiac arrest. 

Surprisingly, the most common complications of GBS are related to the treatment:

Causes of death are most often secondary to the victim's level of care, or more specifically, due to the lack thereof.

 

According to the medical record at N-6  Arlene Berry was admitted at 18:45 hours and had spent 75 minutes in the ER,  as evidenced at A-3.  In all that time, the ED physician, Dr. Spiller, did very little. NO simple blood tests were done or even ordered at that time.  It is also clear that no course of action was charted, marked by a clinically evident inability on the part of the ED physician to adequately make a proper evaluation or even make a provisional diagnosis. In fact, Dr. Spiller had no idea what to look for and chose to play the "wait-and-see" game in the face of life threatening indicators.

Not only did the family physician fail to attend, NO diagnosis or differential diagnosis was made following the patient's admission at that time, or at all. NO protocols were followed. There is absolutely nothing on record to suggest that any Supportive Care & Symptom Control Regimens were ever implemented.

 

A-3  of the record, what I take to be the physician’s diagnostic chart is a total blank. Again, from that record it seems clear that nothing was entered because nothing was done. The same record was filed out-of-sequence. The emergency record at A-4 was also filed out-of-sequence. Interestingly both of these records were dated using a rubber stamp that is consistent with backdating.

The record at A-12, what I take to be physician orders documents a concomitant or concurrent administration of Senokot (laxative), MS Contin (narcotic analgesic), Statex (morphine family),  and Gravol (an anticholingeric agent), including IV solution and additives, the most dangerous of which is the MS Contin, a brand name for "Morphine Sulfate". 

According to the record at A-13, Arlene Berry was given 30 mg (po bid) morphine by nurse McCrank at 2000 hours on May 23rd, the eve of her death in the face of an undiagnosed and undifferentiated condition(s) associated with "abdominal pain". Nurses do not dispense medications to patients without a doctor's order.

 A judicious dose of morphine on standing order to patients with non-traumatic abdominal pain is usually in the range of 05. 

 

The record at N-6 also documents telephone orders received by the hospital from Dr. Jordan at 2030 hours for Stemetil 10mg  by  IV,  4 times daily for "control of nausea", given by the RN, as further evidenced by the physician's orders seen at A-11. 

A typical single dose of Stemetil for a small woman with low body weight is 5mg.

 

  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".

Neurolept-analgesia, which is produced by the combination of an opioid (morphine) and a tranquilizer(prochlorperazine), is defined as a state of CNS depression.

Stemetil, also known as prochlorperazine, is a phenothiazine derivative not be administered in the presence of circulatory collapse, altered states of consciousness or comatose states,  patients with pre-diabetes (borderline or chemical diabetes), including  diabetes mellitus. Stemetil is highly bound to proteins in blood (91-99%) and has a duration of activity from 4 to 6 hours.

Prochlorperazine intoxication or poisoning can also cause deep physiologic depression that resembles and can mimic brain death.

 

Notably, my wife  had also been given penicillin based medicines and sulfonamides such as Bactrim (Septra DS) and CIPRO (cyproflaxin) on the days before her admission; penicillin and sulfa-based antibiotics can cause the body's immune system to react by overstimulation.

Septra DS is an antibacterial agent with a wide spectrum of adversities (difficulty breathing; closing of the throat; swelling of the lips; and unusual bleeding).

Signs and symptoms of overdosage reported with sulfonamides include anorexia, colic, nausea, vomiting, dizziness, headache, fatigue, drowsiness, decreased appetite. Hematuria may also be noted.

Cross-reactions between penicillins and sulfa-drugs including sulfonamides are common triggers of drug-induced GBS serum sickness and fixed drug eruptions. 

 Compare: "fixed drug erruption" with "Toxic Epidermal Necrolysis".

 

Coadministration of narcotic analgesics such as MS Contin with laxitives, ie. Senokot may have additive central nervous system (CNS) and gastrointestinal (GI) system effects which can increase the risk of severe constipation or paralytic ileus,  including CNS depression.

 

"Contin",  is a pharmaceutical industry buzzword for "time-release" or "continuous" release. Additionally, Arlene Berry  had been given Statex (a narcotic: opioid agonist analgesic used to relieve pain) which also belongs to a class of the morphine family. "MS" (morphine sulphate) is often confused  with 'Magnesium Sulphate'. Magnesium Sulfate is used to treat severe constipation.

Severe constipation may also be the result of dehydration (water insufficient to rid body of wastes); can result in fecal compaction and perforation.

 

Overuse of laxitives, or in combination with bisphosphonates or Magnesium Sulfate, or an overdose of magnesium sulphate used to treat severe constipationcan can lead to  hypermagnesemic pseudocoma, which mimics a central brainstem herniation syndrome.

 

The co-administration of a narcotic analgesic and a neuroleptic agent will result in neuroleptanalgesia with drug-induced reduction of oxygen intake, resulting in respiratory depression. 

 Neurolept Analgesia, also called "conscious sedation" refers to the use of major tranquilisers, ie prochlorperazine in conjunction with narcotics such as morphine. 

Respiratory depression represents the principal negative variable introduced with "conscious sedation" and left unrecognized and untreated, is the cause of panic, including most serious complications.

 

The intestinal immune system contains almost 70% of the body's immune cells.

 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.

 

Stemetil is widely distributed into body tissues and fluids. Stemetil undergoes metabolism in the gastric mucosa and on first pass through the liver where it enters the enterohepatic circulation and is excreted chiefly in the feces.

Stemetil can also lead to changes in the blood-brain barrier (BBB), allowing an infectious agent to gain entry to the brain and produce lethal central nervous system (CNS = brain and spinal cord) infection. The scientific literature describe two bacterial factors specific to the meningitis pathogen that thwart the normal protective role of the blood-brain barrier, leading to serious infection.

Further, sugar solution in IV creates gaps in the blood-brain barrier allowing chemicals to enter. Infected material can block the blood vessels to the brain, and Stemetil can help shuttle it directly into the brain and CNS. Once across the blood-brain barrier, the infection enters neural cells, with resultant disruption in cell functioning, perivascular congestion, hemorrhage, and inflammatory response diffusely affecting gray matter disproportionately to white matter.

Blood borne infection in the blood lyse easily. It seems logical to assume that Stemetil would be contraindicated to serious infection for this reason.

Increased sedation is a serious side effect of this type of agent.  Further, phenothiazines have even been reported to trigger diabetes in patients with no previous history of diabetes. Prochlorperazine intoxication or poisoning can also cause deep physiologic depression that resembles and can mimic brain death.

Stemetil poisoning is marked by oversedation, respiratory depression and hypotension.

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.

It is also clear that Dr. Jordan sought to eliminate the symptom "nausea", without his attendance, as evidenced by the phone order "for control of nausea" and without any appropriate blood testing, or addressing any possible underlying causes. 

Further, Dr. Jordan neglected to consider the etiology of the nausea and vomiting as a condition requiring prompt medical intervention. Instead, he elected to give the patient a brain damaging neuroleptic antipsychotic-antiemetic drug without any review of her medical record, and without the benefit of toxicological screening or close monitoring, evidenced at A-21.  Clearly, the etiology of the nausea and vomiting had never been determined,  as evidenced at A-3..

 Morphine and prochlorperazine have a profound impact on bowel motility, often resulting in fecal impaction.

 Notably, antiemetic/antipsychotic drugs, such as Stemetil (prochlorperazine),  can cross the blood-brain barrier taking with it purulent exhudates in the presence of bacterial infection. Purulent exhudates is a medical term  for "pus-producing bacteria", usually leading to serious infection. The most common manifestations are meningitis and brain abscess.  Atypical antipsychotic medications can also trigger diabetes.

The cyst fills with bacteria and pus, and becomes an abscess (chocolate-brown abscess fluid is thought to be highly characteristic of amebic abscess); the earliest amoebic lesions appear as small, yellow  mucoid (yellowish exudate) elevations containing necrotic material where the parasite can be found. The center of an  amebic abscess, consisting of lysed hepatocytes, erythrocytes, bile and fat, may liquify and this necrotic material (sometimes incorrectely called pus) will range in color from yellowish to reddish brown.

If the abscess bursts inside the body, there is a risk of blood poisoning (septicaemia).  Septicemia, is a form of sepsis.

Trapped blood (ie. from an old hemorrhage or occipital bleed) can also lead to the growth of cysts. Patients can be asymptomatic even if the cyst is quite large.

 

The record at 0020 hours seen at N-6 documents the discovery by duty nurses of the patient's "head against the left side bed rail with her feet under the right side rail".  Sensory loss in GBS, if present, takes the form of proprioception (loss of sence of one's own perception of the relative position of neighbouring parts of the body to each other), which is occasionally impaired spontaneously, especially with extreme fatigue. 

The ED physician,  Dr. Spiller was up to assess the patient's condition. Upon examination her eyes were documented as being "sluggish". She was simply repositioned by the nurses,  as evidenced by the record at  N-6.  Her "pupils were dilated at approx. 5 mm"  with "very little reaction to light", and far from getting better she was becoming progressively worse, as evidenced by a sense of urgency seen on the record to the attendance of the patient with increased activity edidenced at  N-6  between  0030  and  0055 hours,  also noted at N-5.  Clearly, from that record and apart from running around the room looking busy and repositioning the patient, nothing was done. It seems clear that the ED physician failed to properly assess the patient's condition, which fell far below an acceptable standard of care. Further, to add insult to injury, NO bloodwork had yet been done and nothing was charted because nothing was yet been started. 

While the clinical feature of 'fixed dilated pupils' is a valuablr clinical sign it does not necessarily mean that the patient has severe brain injury.

 

Guillain-Barré Syndrome is a frightening and disabling disease which strikes suddenly, sometimes with devastating effect. Panic disorder commonly coexists with essential hypertension and the postural tachycardia  syndrome in which blood pressure decreases while heart rate increases.

 Panic, in turn, can stimulate increased ventilatory effort, which can result in more fatigue and increased panic - a vicious cycle.

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

Further, between 0200 hours and 0220 hours the patient's  blood pressure had risen slightly from 150/72 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".

A-26 documents a blood pressure of 162/80  with an SaO2 of 80% at 0220 hours, followed by a lethal drop in blood pressure to 78/70 by 0235 hours,  in which blood pressure  rises or falls significantly, a hallmark feature of orthostatic hypotension.  Orthostatic hypotension is also a hallmark feature of diabetic autonomic neuropathy.

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.

 

Understanding GBS is to see it for the nightmare that it really is. Put yourself in the position of a GBS patient with near total, or complete paralysis, and with most of your senses blunted, unable to move, speak or even open or move your eyes due to a severely paralyzed motor function - you try relentlessly to free yourself until you become overwhelmed by exertional fatigue, or stress, fright and panic that your heart rhythm begins to change rapidly and eradically, marked by hypertension and sinus tachycardia (>90/min) with awareness.

 

What it is like to be conscious but paralyzed and voiceless, relates to the terrifying situation of an intact awareness in a sensitive human being, experiencing frustration, fright, stress and anguish, locked in an immobile body, wondering what is happening.

 

There are numerous material deficiencies in the related medical record of Arlene Berry which manifest a complete lack of internal consistency, ranging from out of sequence records, from the physician's Discharge note seen at A-1 and A-2, which is mared by error, inconsistency, omission, and contradiction, to the nurses Triage, to obviously rewritten, altered, and falsified medical records, taylored to obfuscate the truth, seen between N-1 and N-3  of the nurses notes, with  A-16 and A-17  presenting similarly, including as follows:

A-26  of the record documents a BP (blood pressure) of 78/70 at 0235 hours, while N-5 documents a BP of 98/70 at the very same time, suggestive of copious error.

A-24  documents a heart rate of 174 bpm at 0330 that is consistent with "trauma", while the Ventilation Record documents a heart rate of only 126  at the very same time, a significant difference.

A-4  of the record, what I take to be a Trauma Legend, barely visible in the physician’s notes situated in the lower right hand side of that record, there is an "obliterated" area suggesting a white-out, or perhaps an erasure. From that record it seems clear that relevant information was deliberately withheld, or removed to conceal an event. 

TRAUMA is defined as any insult to the body, clinical or otherwise.

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

N-4 and N-5 present with less than half a page of documentation consistent with deliberate omission, such as 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. More copious error.

N-4  of the record documents that Dr. Jordan was called in at 0225 hours.  A-1 of the record documents "I was called in later that night because the patient had become obtunded",  while the record at  N-2  documents "attempts to pull away to painful stimuli" as late as 0400 hours on May 24th,  being one hour and thirty-five minutes later, according to the record.

Was it the doctor's belief that Arlene Berry  ceased to be a human being after becoming unresponsive following undiagnosed, untreated and/or inappropriately treated conditions?

 

N-10 of the record which documents the patient's bowel routine and urinary elimination pattern for toileting is a complete blank, with the very same information that ought to have been recorded, also omitted  at OP-53 of the record.  

Reduction in blood flow (relative ischemia) impairs oxygen delivery and causes cerebral hypoxia. The hallmark of reperfusion injury after brain ischemia is an "inflamatory reaction" which can result in shock and circulatory collapse, marked by a rapid drop in the blood pressure.

GBS can freeze the breathing muscles with assault on muscle function resulting in episodic and paroxysmal disorders with progression.

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

The same record at N-5  documents a physician "assessments unchanged" at the very same time despite the fact that the patient had already gone into respiratory distress, as evidenced by "Cheyne-Stokes" respirations with periods of "apnea" lasting "5-8 seconds".  

GBS patients exhibit a progressive paralysis that reaches a plateau phase of persistent, unchanging symptoms.

Brief plateau phase then improvement and gradual resolution over weeks to months. Recovery begins 2-4 weeks after progression ceases.

 

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. Other causes include panic attacks.

The record at N-5  documents the respirations as "deep and soaring without constant jaw lift" as early as 0220 hours. A-26 of the record documents "gurgling", and "snoring" and is evidenced in the lower left corner of that record.

Failure to manage the airway with endotracheal intubation when necessary is a medico-legal pitfall.

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 the plastic airway, according to the duty nurse was "to keep the patient from swallowing her tongue".   

 Weakness of tongue and retropharyngeal muscles causes positional airway obstruction; difficulty with protruding tongue and difficulty swallowing indicate that bulbar involvement is significant, which requires that these patients be placed on ventilators in order to breathe.  Snoring, sleep apnea and gasping for breath are part of the same problem.

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. The visual effect is indistinguishable from that associated with stupor.

Stupor is characterized by impairment of the arousal system. In stupor, a person arouses only in response to strong verbal or tactile stimuli, awakens briefly, and then lapses back into a sleep-like state after the stimulation stops.

Some cases of GBS may be so mild that medical attention is never sought, and there are  case reports of patients with some distal control of fingers and toe movements who were only able to move a few fingers and "wiggle" some toes.

In order to functionally communicate, it is necessary for these patients to be motivated and to be able to receive and emit information, be it verbal or otherwise.

 

Paresthesias in GBS occur, spreading proximally but seldom extending past the wrists and ankles.

 

In my opinion, Arlene Berry  appeared to be more paralyzed or blunted  than anything, with the exception of short spasmodic joint contractions  of the right leg which rapidly diminished and became hyporeflexic.

Her condition was  cataleptic-like, characterized by a  profound  hypnotic state, or psychomotor condition of morbid sleep,  such as seen in cataplexy,  neurolepsis,  sleep paralysis, or narcolepsy. 

Underlying causes of catalepsy include severe emotional trauma, and emotional shock. Compare: neuroleptanalgesia (conscious sedation) with a severely paralyzed motor function.   

Although patients with GBS in the setting of preserved consciousness may appear to be completely obtunded, they are technically awake, and fully lucid. But he/she may literally not be able to move a muscle in response. The GBS patient only appears to be unresponsive due to a severely paralysed motor function.  It has been shown that more than half of the time it is the family and not the physician who first realized that the patient was aware.

 Stupor and coma are characterized by impairment of the arousal system. In stupor, a person arouses only in response to strong verbal or tactile stimuli, awakens briefly, and then lapses back into a sleeplike state after the stimulation stops. In coma, a person cannot be roused to consciousness.

With GBS the patient is conscious but unable to respond due to a severely paralysed motor function.

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

Noise heard during any part of the respiratory cycle may indicate airway obstruction or alteration in airway patency.  Patients with neuromuscular disorders have rapid, shallow breathing secondary to severe muscle weakness, which requires that these patients be placed on ventilators in order to breathe.

 

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

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

   Gastrointestinal (GI) bleeding due to stress ulceration in GBS is reported in the literature.

GI bleeding is considered a potential medical emergency. It involves assessing hemodynamic stability, resuscitating the patient as needed, locating the source of the bleed, and treating the underlying cause.

 

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

 

The record at N-4 documents "incontinent blood tinged urine" at 0305 hours. Incontinent "tinged urine" is consistent with severe dehydration, often mistaken for hematuria (blood in urine).  Notably, N-3 of the record documents a "large amount of dilute urine" (polyuria) at  0325 hours, only 20 minutes later. The record at N-2  documents "Foley draining lge amt dilute urine" at 0425 hours, while  N-1 of the record documents  "Foley catheter emptied for 1200cc dilute urine" at 0450 hours that is consistent with iatrogenic fluid overload,  suggestive of diabetes insipidus.

Nothing was done to treat diabetes insipidus (DI).

 Diabetes Insipidus in GBS is caused by a nervous derangement. Overworked emotions associated with 'fear' (panic factor) is the cause in those who are very nervous or frightened, or fluid overload due to an excessive amount of IV fluid infusing to quickly, over a short period of time, or an accumulation of small amounts of extra fluid over a longer period of time.  Signs include  shortness of breath, increased respirations, increased blood pressure. Excessive urine excretion is also a  prominant finding in diabetes.

If a person with diabetes insipidus does not store enough water, their body can become dehydrated.

Dehydration can cause an electrolyte imbalance, dry skin, rapid heart rate and sunken appearance of eyes, ie. the eyes turn cloudy and sink in to be level instead of rounded. The visual effect is indistinguishable from that associated with brain death.  

Severe dehydration initiates a cascade of metabolic derangements that result in progressive dehydration, hyperosmolarity, hyperglycemia, and consequent neurologic derangements. Hyperglycemia is only a component of the overall metabolic derangements. 

The hallmark of hyperosmolar hyperglycemic  state is profound dehydration, marked hyperglycemia, and often some degree of neurologic impairment with mild or no ketosis.

 

Also known as water intoxication,  hyponatremia occurs when the sodium in your blood is diluted by excess water. The body's balance of electrolytes is pushed outside of safe limits, disrupting normal brain function, which causes the brain to swell.  The symptoms of hyponatremia can mimic the symptoms of dehydration, the direct opposite of hyponatremia. Also known as hyperhydration, hyponatremia occurs more often in women than in men.

hyponatremia = METABOLIC.

Autonomic Abnormalities in GBS

 Syndrome of inappropriate antidiuretic hormone (SIADH) occurs in some patients with GBS.

(Parry, 1993, p.15)

 

Autonomic dysfunction in GBS is manifested as tachycardia and mild hypertension in the accute stage and cardiac arrhythmias associated with autonomic dysfunction are a recognized manifestation in Guillain-Barré syndrome.

 

 

Evidence of Na negligence (SIADH)

"morbid and iatrogenic events involving IV salt and water"

 

Na is the chemical symbol for sodium. From natrium, a synonym for sodium. Normal blood sodium level is 135 - 145 milliEquivalents/liter (mEq/L), or in international units, 135 - 145 millimoles/liter (mmol/L).

Acute paralysis in Guillain-Barre syndrome is related to Na negligence.

It results from a deficit of sodium, or surplus of water due to iatrogenic fluid overload. It occurs in patients with Guillian Barre syndrome, meningitis, encephalitis, pneumonia, septicemia, severe malaria, bronchiolitis, RSV infection, or as a direct result of clinical insult.

Rapid correction of hyponatremia can cause osmotic brain demyelination.

 There is also a positive association between blood brain barrier disruption, and osmotically-induced demyelination by exposing substances normally excluded from the brain.  Aseptic meningitis may follow.

Blood-brain barrier (BBB) disruption is usually accompanied by cerebral edema.

A case where cerebral edema and ophthalmoplegia was reversed with administration of mannitol is reported in the literature. 

 

Positive association between blood brain barrier disruption and osmotically-induced demyelination by exposing substances normally excluded from the brain. Hyponatremia results from a deficit of sodium, or surplus of water. It occurs in patyients with meningitis, encephalitis, pneumonia, septicemia, severe malaria, bronchiolitis, RSV infection and Guillian Barre syndrome.

When sodium is lost alone, water flows into the cells, causing cellular swelling and symptoms of water intoxication. These may include anorexia, fatigue, apathy, and muscle contractions or twitching.

SIADH can also be precipitated by certain drugs but is usually the result of morbid and iatrogenic events involving salt and water; iatrogenic interventions and lapses in nutrition and nursing care frequently play in upsetting the homeostatic balance in this patient group. Hyponatremia and hypernatremia can occur.

Hyponatremia is defined as a serum sodium concentration of less than 137 mEq per L (137 mmol per L). Symptoms of severe hyponatremia include nausea, headache, lethargy, and respiratory arrest.

 

 Hypertonic hyponatremia is caused by the accumulation of osmotically active nonelectrolyte solutes, which causes the movement of water from the intracellular compartment to the extracellular fluid.14 This action dilutes the sodium concentration and is usually the result of hyperglycemia. Patients with hyponatremia usually are asymptomatic. Symptoms often do not occur until the serum sodium concentration drops below 125 mEq per L (125 mmol per L). The most common manifestations of hyponatremia are neurologic, the result of swelling of brain cells secondary to intracellular movement of water.

 

SIADH = syndrome of inappropriate antidiuretic hormone secretion; also known as water intoxication, occurs when the sodium in your blood is diluted by excess water. The body's balance of electrolytes is pushed outside of safe limits, disrupting normal brain function.

Circulatory overload can occur if an IV is not regulated and IV fluids infuse too rapidly for the patient's body to handle. Signs of fluid overload include tachycardia, elevated blood pressure, headache, anxiety, wheezing or other signs of respiratory distress

Demyelinating disorders can present with radiological features that mimic brain tumors, or may be the result of extreme intracranial hypertension. Further, brain  demyelination can cause ring enhancement mimicking a neoplasm, or infection on routine imaging.  This is a well known entity to neuropathologists who deal with many obscure pathological entities that may simulate brain neoplasms, such as infection or abscess, for example.

Because of demyelination,  mass lesions that mimic brain tumors on CT or MRI can be misinterpreted as metastatic cancer of the brain. Demyelination, as evidenced by slow conduction velocity and conduction block, are reversible features of the disease. 

 

A-15  documents the 24 hour IV fluid balance record, that  between 1745 hours and 0200 hours was administered as follows:

A-14  documents an  " IV gid prn", meaning that fluid and medication rate of administration to be is given by IV as follows:  "2/3 and 1/3", being a 3.3 % dextrose and 0.3 % sodium chloride @ the rate of 100 cc/hr, as evidenced at A-15. 

The same record documents a total Na of 1000 cc TBA, (to be absorbed), documented  by nurse Bates at 1745 hours;  with a 150 ABS (absorbed) by 1900 hours,  documented by nurse Ferguson, shows 150 cc absorbed over a period of 75 minutes; far exceeds the rate of 100 cc/hr. Anything above 100 cc/hr points to "overly rapid infusion".

Na 850 cc TBA remaining at 1900 hours documented as ABS (absorbed) by 0200 hours, over a period of 7 hours,  resulting in a "surplus" of 150 cc fluid, with an additional 1000 cc TBA, and no further documentation with respect to Na monitoring. The ventillation record at A-16 shows a complete absence of information with respect to "Water Refill".

Hyponatremia results from a "surplus of water" due to Na negligence. Other evidence of fluid overload as indicated by "ascites" due to fluid build-up in the abdomen.

Rapid correction of hyponatremia, even mild hyponatremia, risks neurologic complications (see Fluid and Electrolyte Metabolism: Osmotic demyelination syndrome). Generally, Na should be corrected no faster than 0.5 mEq/L/h. Increase should not exceed 10 mEq/L over the first 24 h. Any identified cause of hyponatremia is treated concurrently.

The record at N-6 documents "IV infusing well". There are no further IV related entries on that record, or any other record, either to indicate when or if the IV was discontinued, or to show that the rate of administration was being monitored, suggestive of patient dumping, or abandonment, with deliberate omission by reason of Na negligence.

The same record documents the use of a No. 20 "Quick Catheter"; signed by nurses Bates, Ferguson, and McCrank.

RN is ultimately  responsible for monitoring rate of infusion.

 

The same record documents a  "hard" IV site in the "R" (right) hand; clot formation due to irritation, of the vein from
solution or medications is the most common cause of a hard IV site. The back of the hand has weaker veins, and is not commonly used for IV antibiotics.

Seriously ill patients require accurate fluid balance monitoring because IV fluid also contains the medication(s). Rapid infusion may also lead to overdosage.

Circulatory overload can occur if IV is not regulated properly and IV fluids infuse too rapidly for the patient's body to handle.

Signs of fluid overload include tachycardia, elevated blood pressure,  dyspnea and other signs of respiratory distress. Neuromuscular disease is another well-known cause of dyspnea.

 

Notably,  Stemetil 10mg  was added to the  IV at 2030 hours. The drug is sedating and a potent vasodilator, which also crosses the blood-brain barrier.   Patients are usually "volume expanded" prior to its use,  often due to negligence,  resulting in hyponatremia due to a surplus of water.

Hyponatremia is diagnosed by measuring serum electrolytes. However, serum Na may be artifactually low when severe hyperglycemia increases osmolality. Water moves out of cells into the ECF. Serum Na concentration falls about 1.6 mEq/L for every 100-mg/dL (5.55-mmol/L) rise in the plasma glucose level above normal. This condition is called translational hyponatremia because no net change in the amount of Na has occurred.

The record at N-4 documents the patient's  "transfer to ICU" at  0320  hours,  while  record at N-3  documents a "congested oral airway" at the very same time. 

A panic attack in severe GBS is capable of producing obstruction or congestion of the breathing passages.  Certainly the inability to breathe properly can be alarming, and many persons will immediately react with anxiety, fear, or panic.

The record at A-24 documents the mechanical charting of the patient's vital signs that commenced recording at 0315 hours. It is interesting to note that the patient's transfer to the ICU had not yet taken place, and that no prior attempt was made by any of the healthcare providers to place the patient in the ICU prior to that time. 

From these records alone it seems clear that the healthcare provider had done too little too late as evidenced by the records at   N-9,  N-10, N-11, including  A-3,  and  A-21.

From the record as a whole, it seems clear that both doctors should have realized  at the onset, the severety of the patient's signs and symptoms and that they were faced with a critically ill young woman who was not responding to treatment. They should ALSO have been acutely aware of the danger. 

Critically ill patients frequently have multiple physiologic derangements that come from a range of possible sources and occur simultaneously.

It is also of interest to note that NO attempt was made by either of the doctors to place the patient in the ICU in a timely manner. Further, the patient's condition remained critical throughout the night and into the small hours of the morning notwithstanding.

N-5 of the medical record  documents a gurgly respirations as evidenced by a "gurgly resps" at 0220 hours, a sign of constriction suggestive of thoracic trauma (patients are often in shock). The same record documents   "deep and soaring and without constant jaw thrust", such as associated with the airway and swollowing difficulty in respiratory compromise.

Gurgling is a bubling sound. It usually  indicates upper airway obstruction from secretions, emesis, or blood.  Gurgling respirations indicate the presence of fluid, usually  blood or vomit or both.

The record at N-4  of the Nurses' Notes documents "incontinent blood tinged urine" at 0305 hours that is consistent with  urinary incontinence (leakage of urine) or  blood tinged urine if bladder infection is also present.  Urinary dysfunction such as  incontinence (leaking) of urine is a prominant finding in GBS patients due to autonomic abnormalities. Incontinence is loss of bladder control, and is also a very serious side effect of antipsychotic medications. Further, during episodes of  hypokalemic periodic paralyses urinary output is decreased  during the attack because water accumulates intracellularly in muscles.

Dark, concentrated urine in decreasing amounts (incontinent tinged urine)is also a prominant finding in patients with high blood sugar, including dehydration.

A-8  of the related record documents "patient was unconscious with respirations of approximately 30 and laboured", that is consistent with dyspnea - difficult or labored breathing.  Dyspnea is breathlessness due to high filling pressures and pulmonary congestion/edema, i.e. shortness of breath, a smothering feeling, inability to get enough air, and suffocation. Breathing may become  laboured and difficult; laboured breathing is the hallmark of respiratory distress and respiratory failure due to paralysis of the diaphragm.

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. Babinski’s sign is a prominent finding in Bickerstaff’s brainstem encephalitis (BBE).  Limb weakness in GBS is nearly always bilateral (Parry, 1993).

The lower limb is often ischemic in diabetes. Fecal impaction as a cause of acute lower limb ischemia is also reported in PubMed.

Reflex changes in GBS

Reflexes become absent or hyporeflexic early in the disease course and represent a major clinical finding on examination of the patient with GBS. Pathologic reflexes, such as Babinski, can also become absent. Hypotonia may also be observed with significant weakness.

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.

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 hourss, according to the record at N-3.  The same record documents the time of the patient's intubation by Dr. Jordan at 0325 hours, 5 minutes later.  What I take to be the Ventilation Record at A-17 documents the arrival in the ICU of the hospital's ventilatory therapist, Helene Studholme  at 0330 hours,  after being  "called in for patient requiring ventilation". From these records, it is clear that either the ventilatory therapist was not present at the time of the intubation procedure because she did not show up until 5 minutes later, or that the intubation did in fact take place at an earlier time, such as 0320.

Notably, the record at A-24 documents a HR (heart rate) of 174 bpm at 0320 hours that is consistent with  an "awake intubation", (any suspicion of difficulty intubating, for any reason), marked by panic with "awareness".

To illustrate, the Vital Signs Record at A-24  documents a heart rate of 174 bpm at 0330 that is consistent with "trauma", while the Ventilation Record seen at A-16 documents a heart rate of only 126 at the very same time, a significant difference, suggesting that the timeline for that event was in fact altered by the Ventilatory Therapist to obfuscate iatrogenic trauma related injury. The Vital Signs Record is a mechanical record with a print time, while the Ventilation Record is a handwritten account, mared by having been rewritten. Which is more likely to make copious errors or downplay an event by telling lies?

There is nothing on record to suggest that anesthesia was or wasn't given to prepare the patient for the intubation procedure.

 

The earliest indication of shock is an increase in heart rate (HR).

 

 

 

The very act of breathing is entirely neurologic. In fact every component of breathing (the lifelong automatic cycling of inspiration, the transmission of coordinated nerve impulses to and from the respiratory muscles, the translation of systemic influences such as acidosis to the neuromuscular apparatus of the diaphragm) is under neural control.  Certainly the inability to breathe properly can be alarming, and many persons will immediately react with severe anxiety, fear, or panic which may accompany the progressive phase in patients with GBS. Patients who are paralyzed by the illness, are mentally alert and very  fearful.

GBS can, very rarely, present with coma and absent brainstem reflexes. Such patients are NOT brain dead; their brains and sense of hearing and smell work perfectly well, and the patient is alert and conscious of what is going on around him or her. But he/she may literally not be able to move a muscle in response.

Although patients with GBS in the setting of preserved consciousness may appear to be completely obtunded, they are "fully lucid". They only appear to be unresponsive, with a seemingly apparent reduction in alertness and arousal, due to a severely paralysed motor function.

According to Dr. Jordan "the intubation proceeded uneventfully", while  N-2 of the record documents the ET (endotrachial tube) "pulled back 4 cm" at 0425 hours. From that record it seems clear that the endotrachial tube had been malpositioned for almost one full hour before the error was discovered by one of the nurses, as evidenced by the record at N-2;  infers a failure of the part of the healthcare providers to identify an incorrectly placed airway.  Both myself and the patient's foster brother were present to witness that event.  Malpositioning of ET tube can cause airway obstruction and may also result in tissue trauma, and bleeding.

When an endotrachial tube is misplaced in the esophagus and misplacement is detected late, a compromise of the patient's safety can be significant.

 

A-12 documents a blood pressure  of 163/117 at 0320 hours that by 0345 hours dropped to 85/52, following intubation.

A-12 of the medical record documents a  blood pressure of 163/117 bpm at 03:20 hours that by 03:45 hours had dropped to 85/58, and again to 85/52 bpm by 3:52 hours,  over a span of some 7 minutes, as evidenced at  N-2 in the Nurses' Notes.

The same record documents "patient  suctioned down ET tube several times for small amount of brownish mucous",  while A-17  documents "being suctioned for moderate amounts of coffee-ground emesis by RN" at 0330 hours.   

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.

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 physician's Lab Work Summary at A-19  documents  the charting of a course of Hematology (bloodwork) and Coagulation. The same record documents a Fibrinogen level of 4.67 H (the normal range is 2.00-4.00). Serum fibrinogen levels in a safe range is <300 mg/dL.

The plasma fibrinogen level appears to reflect disease activity in acute Guillain-Barré syndrome. In fact, ongoing activity of Guillain-Barré syndrome may be reflected by a persistently elevated fibrinogen level. Further, elevated levels may also be seen with TRAUMA of any kind.

When blood protein is high, CSF usually clots because of the presence of increased fibrinogen.  From that record it seems clear that due to Dr. Jordan's mindless and promiscuous use of inappropriate lab settings, or other negligence, he triggered a coagulation cascade of spontaneous slugging of the blood sending numerous  "blood-clots", including infectious material to his patient's brain.  Multiple intracerebral hematomas (blood-clots) can mimic brain metastases. Cerebrovascular diseases, demyelinating processes, inflammatory or infectious diseases, iespecially  pyogenic brain abscesses with subdural empyema and other miscellaneous diseases can show similar imaging findings.

 A-19  documents a  D-dimer  test level of 1000 H (<500), suggests "thrombosis".  Thrombosis signifies the formation of  blood clotting within vessels of the brain or neck. People  who are suffering from a severe infection are more likely to develop dangerous blood clots, but inappropriate combinations of medications or treatment can sometimes be the worst offenders.

The Cardiac Index at A-18  documents the patient's ventillation rate at 129 bpm (breaths per minute) at 0417 hours,  with heart and breath rate increased.

Increased  heart and breath rate can suggest clinical insult, such as caused or worsened by medications, resulting in oxygen deprivation.

The Cardiac Index documents the patient’s age at "55 years", she was only 41 at the time of her death; can imply negligence, or even patient record swapping.

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

The aPTT is typically elevated in 90% of those with coagulopathy, an increased bleeding tendency due to decreased hepatic synthesis of clotting factor, i.e. with prothrombin (a protein involved in clotting).

 A-19  documents a "PLT ESTIMATE" - "MOD INCREASE" confirming a moderate increase in platelet aggregation activity (blood platelets sticking together), indicating that blood thinners may be needed to prevent blood clots.

From the record nothing was done to correct coagulopathy.

The ambulance call report seen at  N-7, of the Nurses' Notes documents that the patient was intubated and vented and that she was seen to be "stable",  but that she appeared to be "pale, dry and cool".

In patients with GBS, the skin may become pale and dry, and sweating may become reduced. Body temperature can be marred by the effects of drug-induced temperature dysregulation, which can suppress sweating, causing central nervous system impairment, often resulting in an afebrile state. 

Cool, dry skin can also suggest late sepsis, a prominant finding with iatrogenic neglect.

 

Hemodynamic instability has also been defined more broadly as global or regional perfusion that is not adequate to support normal organ function. This definition recognizes the obligation to insure adequate organ perfusion during the flaccid period in patients with GBS.

According to the Nurses' Notes at  N-1  of the record the patient was given  Gravol 50 mg x 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".

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.

Following her transfer to Sudbury on May 24th of 2000,  Arlene Berry's remains was returned to Kirkland Lake several days after family had been notified of her death via her foster brother acting as a family contact, who was notified by phone.

On seeing the deceased vicim, her eyes were "sunken in appearance", with swelling and distortion of the face, eyes, and lips, as was the case, marked by a rash-like redness  resembling a sunburn with "blistering" wrinkles in the skin in the area just below the right eye, consistent with a delayed hypersensitivity reaction, or fixed drug-eruption, evidenced by all who attended Arlene Berry's viewing at the Monette Funeral Chapel in Kirkland Lake.

 It is now believed that Arlene Berry's death was provoked and that her eyes were taken by Drs. Sauvé, and Adegbite at the Sudbury Regional Hospital, upon remote third party consent (foster brother), utilizing deception to obtain that consent, by-passing permission from Arlene Berry's immediate family, ie, her de facto common-law spouse and her children.  Only biased clinicians might provide less aggressive medical treatment and influence the family in inappropriate ways.  Indeed,  the fraudulent taking of the patient's eyes in the manner in which it was done can only be construed as theft.

 From the information at hand it seems clear that Drs. Sauve and Adegbite sought to open  the way, under misleading conditions (influence of drugs, and metabolic disturbances) to organ donation from brain death. The diagnosis of brain death allows organ donation or withdrawal of life support. Certifying brain death to cover-up medical blunders or to increase organ donations constitutes murder.

At a first meeting with the coroner held at the OPP Detachment in Kirkland Lake sometime in July of 2001, Dr. Barry A. McLellan, who was the Regional Supervising Coroner for northeastern Ontario at the time admitted to family that there was "no evidence on record to suggest matastasis". 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 several days later.  It shows multiple lesions of undetermined origin. The pathogenesis of these yet undetermined lesions remaines unclear but a metabolic disorder seems the most plausible pathological factor.

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

Demyelinating diseases Lesions (2 cm or more) of demyelinating plaque with mass-like features are well documented in multiple sclerosis (MS), and other primarily demyelinating diseases, such as myelinoclastic diffuse sclerosis (Shilder’s disease) and acute disseminated encephalomyelitis (ADEM), can manifest as tumefactive lesions.  A very helpful feature is the presence of other lesions, providing an overall picture consistent with MS.

A-1 of the record also documents "she died several days later with numerous metastatic lesions to her brain".

According to her death certificate, Arlene Berry died May 24th of 2000, the very same day she was transferred out to Sudbury. As to the cause of death, according to a Dr. Sauve in Sudbury, she died meeting "brain death" criteria.  No attempt to diagnose was made at that time, or at all. No pathalogical reason was given for the declaration of brain death. No process of exclusion was undertaken without which a diagnosis of brain-death should never have been considered. No autopsy was performed. No appropriate period of observation and/or trial of therapy was ever undertaken. In fact, Arlene Berry was rushed to her death within five and one-half hours of her departure from Kirkland Lake to Sudbury, some 210 miles away.

One might ask how much time did these medical dolts spend assessing the patient before pulling the plug?

Although many conditions can mimic brain death clinically upon examination, without excluding them you will KILL a person by homicide, or criminal negligence, despite the reversibility of brain damage.

Brain death is defined as the irreversible cessation of function of the entire brain with three specific criteria: 1) coma, 2) absent brainstem reflexes and 3) apnea. In addition to these clinical criteria, there are important prerequisites:

1) NO intoxication or poisoning, 2) NO core temperature greater than 32 degrees Celsius, 3) clinical or neuroimaging evidence of acute central nervous system catastrophe and 4) absence of confounding medical conditions such as severe electrolyte, acid-base, or endocrine disturbances.

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

Notably the Sudbury doctors involved were a part of an organ harvesting and transplantation team.

 It was Dr. Sauve who, utilizing deception, sought to obtain permission from a remote party to obtain the victim's eyes,  without immediate family knowledge or consent.

Fulminant Guillain-Barré syndrome (GBS) is a rapidly progressive form of polyneuropathy (damage to many nerves) in which patients demonstrate eventual flaccid quadriplegia and an absence of brainstem function. Most patients present after a mild upper respiratory or gastrointestinal illness and while some may have nondiagnostic cerebral imaging studies, others may display radiological abnormalities mimicking malignant brain tumors.

Polyneuropathy is the simultaneous malfunction of many peripheral nerves throughout the body.  

A patient with fulminant Guillain-Barre syndrome can rapidly develop pupillary denervation, loss of all brain stem reflexes and a complete flaccid quadriparesis.

  Polyneuropathy often affects the nerves of the autonomic nervous system, which controls involuntary functions in the body (such as blood pressure, heart rate, digestion, salivation, and urination). Typical symptoms are constipation, loss of bowel or bladder control (leading to fecal or urinary incontinence), sexual dysfunction, and fluctuating blood pressure—most notably a sudden fall in blood pressure when a person stands up (orthostatic hypotension). The skin may become pale and dry, and sweating may be reduced.

Careful control of blood sugar levels may slow progression of the disorder and occasionally relieves symptoms.

Fulminant GBS can rapidly progress to a pseudocoma state resembling acute unconsciousness, but with self-awareness preserved.

 

 Recognition of fulminant GBS  is important to prevent inappropriate declaration of brain death or withdrawal of life support in the face of potentially reversible causes.

 

 Endocrine gland dysfunction in GBS is due to lack of tissue response. Endocrine responses include reactions to stress or the flight or fight response.

 

Guillain Barré syndrome mimicking brainstem death is reported in J Neurol Sci 1993; 120: 115–7.[CrossRef][ISI][Medline].

Condition called cerebral hypoxia or cerebral ischemia, is the direct result of oxygen deprivation to the brain cells. If proper balance is not restored or corrected in a timely manner, the heart and lungs may fail and the brain will literally begin to suffocate. After several minutes of total oxygen deprivation, the brain may not be able to recover any meaningful function. The autonomic system controlling the heart and lungs fails next, leading to the ultimate cause of death, being oxygen deprivation of the brain cells, akin to "asphyxia".

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. NO biopsy was done (a biopsy, is required for obtaining tissue for pathological confirmation of the diagnosis).

The solitary lesion is also consistent in appearance with an abscess secondary to an occipital dermoid cyst, or early stage cerebritis during/after capsule formation in the early stage of abscess development. Rupture of a dermoid and leakage of a cyst contents into a ventricle or subarachnoid space may produce an epidymitis or meningitis respectively. Further, capsules can rupture resulting in the formation of multiple abscesses.

Multiple abscesses of the brain are an increasingly aggressive iatrogenic disorder.

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 origin.

The occipital lobes interpret vision. Brain tumors are more solid/dense and therefore are usually associated with multi-focal deficits; tumors of the occipital lobe usually produce homonymous hemianopia or partial visual field deficits.  Had the lesion been a recent tumor, there would have been onset visual misperception in half of one or both visual fields, with visual impairment and subsequent loss of vision with evolution, prior to hospital admission. That did not happen. Even multiple brain abscesses may not cause focal deficit to suggest their presence.

Non-neoplastic demyelinating processes of the brain with ring enhancing lesions and mass effect on MRI imaging, mimicking malignant brain tumors, are rare phenomena. The radiologic appearance of demyelinating pseudotumors as contrast-enhancing solitary masses that mimic tumor is well documented.

It seems clear that this was NOT a case of metastatic tumors of the brain, but rather a clear cut case of abscess formation,  or tumor-like masses of demyelination or granulocytes that mimic brain tumors.  Further, with multiple abscesses the meninges typically show a purulent exudate that obscures the sulci making radiographic appearance of microabscesses less visible, hence they are "not well opacified". 

 Granulocytes, which are cancer killing cells (destroying tumors), turn black as they die.

Morbidity due to a brain abscess generally results from brain herniation due to mass effect, the result of iatrogenic neglect, or substandard care.

No autopsy was performed. Further, a family request for a formal inquest was also denied.  Dr. McLellan concluded that Arlene Berry had died of natural causes suggestive of metastatic CA (cancer) of the brain with multiple brain tumors after eliciting what can only be construed as a most questionable opinion from one of his fellow colleagues believed to be associated with the Sunnybrook Health Sciences Centre, where McLellan  spearheaded the North Telehealth Network. The medical record of Arlene Berry for May 23rd and 24th of 2000, tells a very different story from the opinion postulated.

CAVEAT: Eleven percent of mass lesions in cancer patients are not metastases; mass lesions that can masquerade as brain metastasis include abscess (20%) and granuloma (less common and mostly associated with mycobacterial or fungal infection). The commonly observed deficits observed in CNS infection include weakness on one side of the body (hemiparesis), impaired speech production (dysphasia), visual field deficits (may or may not be present), and an inability to smoothly coordinate muscle movements, such as during walking (ataxia).

Patients with a dioagnosis of primary or metastic brain tumor(s) associated with a CNS event should have a meticulous review of their history for other possible causes.

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

Cerebrovascular diseases, demyelinating processes, inflammatory or infectious diseases, and other miscellaneous diseases can show similar imaging findings. Many non-neoplastic neurological diseases can mimic brain neoplasms on neuroimaging or on histological examination, including multiple sclerosis, stroke, pyogenic abscess, toxoplasmosis, tuberculosis, cysticercosis, fungal infections, syphilis, sarcoidosis, Behçet disease, radiation necrosis, venous thrombosis, and others.

Multiple intracerebral hematomas can also mimic brain metastases.

 

 

Questionable Opinion

 


 

 


The opinionated author (whose signature was erased) perceives himself to be expert in his field. Believed to be a neurosurgeon, he is generally lacking. The bald truth is that specialists in a given field are not always expert in that field.  For the record, his opinion remains unsubstantiated. He also failed to provide any evidence whatsoever which might support a finding of metastatic CA of the brain. Further, a paltry CT scan does NOT provide conclusive proof of metastatic brain tumors. For that it takes a biopsy and in this case that was never done. Therefore the true nature of the lesions were never established. Nor does a CT  provide conclusive proof of  brain death.  In fact the author who rendered the opinion suggesting metastatic cancer is pretty much off-the-wall; what one might expect from a "hand-picked" self-interest cash for comment shill, or first year medical student who is thus unworthy of belief. 

Further, the opinions expressed by the nameless author admits that his opinion "does not  take into account all the facts and circumstances surrounding the patient's death".  Such a disclaimer also raises doubt about the accuracy of the clinical diagnosis of brain death.   He bases his opinion on assumption, while ignoring the facts. Obviously he did not take the time to study the patient's medical record.  Instead he opted to tailor or lard his report to justify the opinion that was, in his opinion , being sought by Dr. McLellan for the sake of expediency. This infers a blatant attempt by all concerned to obfuscate the truth.  A finding of possible meningitis with abscess of the brain and/or multiple intracerebral hematomas would have given more credibility to his opinion. In fact, the very 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.

Further, with multiple abscesses the meninges typically show a purulent exudate that obscures the sulci making radiographic appearance of microabscesses less visible, hence they are not well opacified.  In severe meningitis, the basal cisterns may become completely obliterated and that appears to be what happened here. Rapid deterioration is an invariable accompaniment of an untreated condition, in this case,  an undiagnosed case of fulminant GBS with overlaping meningitis, in which  rapid progress of the disease may actually be displaying a pronounced "blood-brain barrier breach", characterized clinically by  "rapid evolution", the result of totally inappropriate treatment, and medications which can breach blood-brain barrier integrity, ie. the drug Stemetil. 

Breakdown of the blood-brain barrier usually precedes inflammatory demyelination. 

GBS is often associated with cerebrospinal meningitis and encephalitis.

Coma in GBS is rare and is the symptom of cerebrospinal meningitis and encephalitis. The clinical manifestations of this condition included areflexia in the cranial and spinal nerves as well as apnoea.

 Cisterns may contain pus in cases of meningitis or other inflammatory conditions, such as sarcoid, or demyelination.

Any medical professional who, in rendering his opinion as to a cause of death,  volunteers his unsolicited opinion as to another doctor’s conduct or standard of care in the face of overwhelming evidence to the contrary,  finding in favour of his fellow colleague(s),  invites being labeled  retrospectively with the most nefarious motives.

Although two physicians with experience and expertise must be responsible for the declaration of brain death, and a neurologic condition capable of causing brain death is a mandatory prerequisite to the diagnosis of brain death, there are reports in the literature of conditions that mimic brain death or that provide examples of the mistaken diagnosis of brain death.

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

 Guillain-Barré syndrome (GBS) is a group of autoimmune syndromes consisting of demyelinating and acute axonal degenerating forms of the disease.

Demyelination is a classic feature of the Guillain-Barré Syndrome.

  Metabolic  impairment causes demyelination or axonal degeneration.

    Demyelinating disorders can present with radiological features or "tumor-like" masses that "mimic brain tumors".  Axonal degeneration secondary to severe demyelination may "mimic brain death".

Fulminant cases of Guillain-Barré syndrome have been reported in which a rapid deterioration evolves to a clinical state "resembling brain death".

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

Acute polyneuropathy has many causes. It may be caused by an infection involving a toxin produced by bacteria, certain drugs such as sulfonamides, or by an autoimmune reaction as in Guillain-Barré syndrome. 

With diabetic neuropathy something also interferres with the body's nerve pathways so that nerve impulses are no longer transmitted properly.

 

A horrific death.

Canadian standards do not test function of the "entire brain", and there is sound evidence that many individuals who meet the clinical criteria of brain death continue to have some cortical, subcortical, or brain stem function. Many patients diagnosed as brain dead do not have hemodynamic collapse, they have physical findings such as bowel sounds, and are reported to have autonomic reflexes (tachycardia and hypertension) at the time of organ retrieval, suggesting a horrific death.

The clinical diagnosis of brain death in this case was made in the presence of metabolic derangements and endocrine abnormalities and constitutes an act of wanton and reckless disregard for human life.

There have been many challenges to the several concepts of "brain death" and the means of their diagnosis worldwide (vide infra). Indeed, it seems that there is now an emerging consensus that "brain death" diagnosed by any of the protocols in current use worldwide is "not death."

After the diagnosis of brain death, the focus of patient care shifts from interventions aimed at saving the patient's life to interventions aimed at maintaining viability of potentially transplantable organs. Given that current clinical testing does not assess subcortical brain function, ‘whole brain death’ cannot be conclusively identified at the bedside by using clinical criteria, and most certainly not on the basis of a paltry CT scan. The CT is useful only in pretty severe cases, such as head trauma and/or during the few days after an anoxic (lack of oxygen) brain injury and also in cases where there has been a massive stroke. If the question is ischemic injury [brain damage caused by lack of blood/oxygen to part of the brain] you want an MRI and PET.

For subsequent evaluation of brain injury, especially brain death, the CT is pretty much useless.

Many Ontario physicians actively involved in the identification of brain death, if the truth be known,  are unable to identify the requisite diagnostic components of brain death, and/or are unable to apply the criteria correctly.  Some physicians will take advantage of the situation to perpetrate a medical murder in order to harvest organs from potential donors, while others will simply declare "brain death" in order to avoid liability for medical wrongdoing.

Organ transplantation is premised on professional and public acceptance that the donor is dead and that the cessation of all brain function persists for an appropriate period of observation. The diagnosis of brain death allows organ donation or withdrawal of    life support. The diagnosis of brain death is dependent upon the exclusion of certain medical conditions without which the diagnosis of brain-death cannot be considered and influence of medications is one of them. 

 

Brain death declaration may be described as an esoteric creation of neurologists and neurosurgeons who are seeking to speed up death for the purposes of an organ harvest/transplant.

 In this case, the harried and hurried  physicians did not rely on those esoteric criteria in pronouncing the patient  "dead."  They  simply used the questionable "brain death criteria"  (based on a paltry CT after withdrawal of ventillatory support) as a pretext to operate and remove their patient's eyes while she was still very much alive.

 

There are numerous reports of brain death declaration where the criteria were deliberately misrepresented, or obfuscated in an attempt to retrieve an organ for transplantation, as in this case.  

Status Code 0, or No Code.

In my opinion, Arlene Berry's death was premeditated, as evidenced by the physician's documented status  "Code 0", and Dr. McLellan knowingly returned a false finding for which he remains to be held to account. From the facts of this case it seems clear that this moral compass isn't such a straight arrow after all.

 

The Arlene Berry Death Coverup!

Medical murder/partners in crime

 

         

JORDAN, Edward Henry             McLellan, Barry A.             Spiller, Mark Arthur 

 

In a letter to the College of Physicians and Surgeons of Ontario dated November 28, 2000,  Dr. Jordan writes  "discussed the situation with family members and a decision was made to intubate Ms. Berry",  while the Ambulance Call Report seen at N-7 documents an unsigned "Status Code 0", or endorsement of a No Code by proxy.

This is an order akin to a 'DNR' denying medical intervention, in this case by passing-the-buck together with all the possible blame.

 

Patient condition "Status Code Zero" taken from CMAJ articles, is used to describe a "dead" patient condition. The Yale Law Journal, Vol. 93, No. 2 (Dec., 1983),  pp. 362-383,  criticizes questionable hospital policies "that resort to third party adjudications in No-Code decision making", and provides insight into the assigning of a "no-code order" instructing personnel "not to attempt resuscitation", as in this case.

Looking over the chart it is clear that obtaining a 'no code' status in the face of immune mediated adversities by reason of Dr. Jordan's and Dr. Spiller's failure to recognise and treat an emergency situation accordingly, and by reason of Dr. Jordan's failure to attend in a timely manner was the next essential step for these two negligent physicians in executing Arlene Berry's death in order to avoid liability issues.

CJNS-Guidelines for the Diagnosis of Brain Death

Brain Death:Inconsistencies

 

The Criminal Code of Canada  regards euthanasia, whether passive or active, as culpable homicide, or murder:  A culpable homicide is defined as murder "where the person who causes the death of a human being means to cause his death" (s. 229, Criminal Code of Canada).  Unless the law has changed in recent years,  euthanasia carries a fixed, minimum penalty of 10 years in prison.

The 'no code' as evidenced in this case by a "Status Code 0" was ordered by Drs. Jordan, and Spiller, without family knowledge or consent when the patient's condition began to rapidly deteriorate following a whole chain of medical negligence and substandard care that is nothing short of criminal.

With the help of Dr. Mark Arthur Spiller (who admitted Arlene Berry to the Kirkland and District Hospital on the evening of May 23rd), a cross-covering physician working the ER with Dr. Jordan on a rotational basis,  these two unscrupulous physicians  were able to recruit two of their equally unscrupulous Sudbury colleagues to complete their dirty work at arms length. Interestingly, Dr. Spiller had been a local appointed coroner working under Dr. McLellan at the time, and also a classmate of Dr. Stephane Sauve, one of the Sudbury doctors involved in this medical homicide.

 

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

 

Within a few hours following her transfer from the Kirkland and District Hospital to the Sudbury Regional Hospital Arlene Berry was declared as having met with 'brain death criteria' ,  while under the care of Drs. Sauve and Adegbite. Her remains were kept in Sudbury for several days prior to being returned to Kirkland Lake.

Withholding life sustaining treatment from an undiagnosed patient with concurrent  hyperglycemia, hypokalemia and electrolyte abnormalities in combination with a severely paralysed 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. Turning off a respirator is a form of passive euthanasia that is practiced by doctors with a family's consent. Turn off the respirator and in the natural course of affairs the patient dies from lack of oxygen.

To practice euthenasia  by withdrawing life support to a critically ill patient is a medical homicide (to kill or destroy by preventing access of air or oxygen).

 

Passive euthenasia involves an allowing of "nature to take its course".   Active euthenasia consists of killing someone (to do acts causing death), or by choosing not to act is also an act, which determines the course and the outcome of events.

An act of wanton and reckless disregard for human life is an act of criminal negligence, in this case, causing death.

 

 

 
Coroner's Report  

Was this Dr. McLellan's way of exonerating those responsible for Arlene Berry's death in order to shield the local appointed coroner (working under him at that time) from liability? Or was it just a blatant attempt on his part to shield his fellow colleagues from absolute disgrace?
 

The Medical Record of Arlene Berry

May 2000

KDH Records Department

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