The Arlene Berry Case</</H1>

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INVESTIGATIVE REPORT

Arlene Berry died suddenly and unexpectedly at the age of 41 less than 24 hours after being admitted to the Kirkland & District Hospital. She presented initially with flu-like symptoms that have since been thoroughly researched and computer traced to the common but unpleasant side effects of a post-operative course of radiation therapy, and chemotherapy, suggestive of iatrogenic hepatic encephalopathy (HE), i.e. liver encephalopathy, or toxic hepatitis. She was transferred to the Sudbury Regional Hospital only hours before she died. No autopsy was performed. Arlene Berry became the victim of a horrific chain of negligence, as evidenced by her medical record from the Kirkland and District Hospital for May 23 rd, and May 24 th of 2000.

FOREWARD

Hepatic means "of the liver" and Encephalopathy means "a disorder of the brain."

Submit that predisposing factors in hepatic encephalopathy include a history of blood in urine (hematuria) or stool (stools-bloody), GI bleeding is the most serious source of bloody stools. opiate use, infection, GI bleeding, dehydration or electrolyte abnormalities. See Common Electrolyte Disturbances in the ED. Compare azotemia. The hallmark test is the serum BUN (blood urea nitrogen) level. See also hepatic failure.

Hepatic encephalopathy (HE) is a syndrome of impaired brain function due to liver failure. Iatrogenic HE (Hepatic Encephalopathy) thus describes a part of this syndrome which is precipitated or worsened by medical procedures or treatments. Iatrogenic hepatic encephalopathy (HE) is defined by the occurrence of brain dysfunction as a direct consequence of a medical intervention (procedures, drugs) in a previously asymptomatic patient with liver disease. The term iatrogenic HE could also be used if a medical therapy or the concomitant effect of medications cause severe liver disease complicated by HE (ie. drug-induced acute liver failure, dysfunction, or impairment. Also some drugs may affect brain function in a manner indistinguishable from HE. Compare drug induced hepatitis.

The liver metabolizes and detoxifies digestive products brought from the intestine by the portal vein. If the liver function becomes impaired the resulting toxic effect on the brain produces the encephalopathy. The complications of acute liver failure are numerous and include: sepsis, gastro-intestinal bleeding, cerebral oedema, renal and cardiac failure. The management of cerebral oedema is critical for survival. Compare portal systemic encephalopathy.

People who contract hepatitis typically develop flu-like symptoms within 10-40 days of exposure (the acute stage). They experience low-grade fever, muscle aches, joint pain, headaches, malaise, anorexia, fatigue and abdominal pain. It is not uncommon for post-surgical patients to become infected. Compare liver cirrhosis. See signs and symptoms of hepatic dysfunction. Cancer treatments such as antineoplastic drugs or radiation therapy can also cause liver damage with mixed forms of hepatic dysfunction. In fact, flu-like and GI illness are common but unpleasant side effects of radiation therapy. Further, some radiation patients may report bloody stools after receiving treatment.

“Acute side effects of radiation therapy occurs during and up to one month after radiotherapy and is due to a disruption of the blood-brain barrier.” Compare Benign Intracranial Hypertension. They result from an increase in cerebral oedema, swelling of the brain. Compare RADIATION NECROSIS, and also Central nervous system syndromes secondary to radiotherapy.

“Acute encephalopathy causes headaches, nausea, vomiting, sleepiness, confusion, and many other neurologic symptoms. Although acute encephalopathy usually develops after the first or second radiation treatment, it is possible for it to occur two to four months later. (Subak-Sharpe, Holleb, M.D., 1987)”.

“Acute encephalopathy consisting of headache, nausea and vomiting, somnolence, and worsening neurological signs may accompany the first or second radiation fraction, particularly when increased intracranial pressure has been inadequately treated with corticosteroids. The encephalopathy lessens with subsequent fractions and after treatment with corticosteroids.” Compare Intestinal Radiation Injury.

Also, patients with hepatitis C can have normal liver enzyme , and still have liver disease, i.e. inflamation of the liver. Compare “compensated" cirrhosis in which patient’s with early stage cirrhosis may not have any symptoms or laboratory test abnormalities., see also liver encephalopathy. Many cases of hepatitis go undiagnosed because the disease is mistaken for the flu or because there are no symptoms at all. Additionally, hepatic encephalopathy can also occur with non-cirrhotic forms of portal hypertension.

Acetaminophen (Tylenol) long term in doses as low as 3g daily can produce a chronic hepatitis-like picture that mimics liver disease in which liver function tests are typically unremarkable. Further, Hepatotoxicity is associated with acetaminophen poisoning. It is of particular interest to note that drugs are implicated in one quarter of patients with hepatic encephalopathy. Another quarter of cases are precipitated by haemorrhage in the gastrointestinal tract. Medication effects and other systemic diseases as causes mandate a thorough drug history as most all Drugs are an important cause of liver damage.

Toxic hepatitis is an inflammation of the liver caused by chemicals. Many chemicals that are intentionally or unintentionally inhaled or consumed can have toxic effects on the liver. Among these chemicals are drugs, industrial solvents and pollutants. Virtually every drug imaginable has at one time or another been indicated as a cause of toxic hepatitis. Compare SYMPTOMS OF HEPATITIS C . Compare also the medical record of Arlene Berry for May 23rd and 24th of 2000.

These are the facts:

In December of 1999, Arlene Berry was sent to Timmins where she was diagnosed with carcinoma of the left main bronchus with residual CA of the aorta due to a complete collapse of the left lung. Her family doctor, Edward Henry Jordan , misdiagnosed her and had been treating her assumptively for “bronchitis.” It took another doctor to order appropriate testing.

On January 13, 2000 she was admitted to the Timmins & District Hospital under the care of Dr. Claudio De La Rocha, and a left lung pneumonectomy was performed. She was released 5 days later. Arlene Berry was then referred to the Regional Cancer Treatment Center situated at the Sudbury Regional Hospital, Laurentian Site (Sudbury) for consideration of radiation therapy under the care of Dr. Hugh Prichard, a radiation oncologist. By the end of April of 2000 she had completed a 5 week post-operative course of radiotherapy. In light of this treatment her condition was seen to be stable. Post-operative testing results were seen to be very encouraging. From that treatment and testing it seems clear that she had every reason to expect a partial remission, or stable condition. At no time was she educated or instructed to be on the alert for, or to quickly report flu-like or GI (gastrointestinal) illness associated with the common but unpleasant side effects of her radiation therapy. Submit that when a doctor relinquishes the care of his patient to another doctor, it is incumbent upon that doctor to take necessary steps to ensure the continued care of that patient which Dr. Prichard neglected to do, tantamount to criminal negligence causing bodily harm. Following her post-operative course of radiation therapy and at all times material to her death, Arlene H. Berry had been suffering from undiagnosed and untreated increased intracranial pressure associated with side effects of radiation therapy and chemotherapy while under the care of Dr. Edward H. Jordan, her family doctor.

Arlene Berry had a left lung pneumonectomy, at the Timmins & District Hospital on January 13th of 2000 due to a complete collapse of the left lung. She was released 5 days later. On or about March 16th she underwent follow-up testing at the same hospital. By the end of April 2000 she had completed a post-operative course of radiation therapy, also know as nuclear medicine . Among other medications she had been prescribed morphine for pain management. She was a small woman with a low body weight and although she had a diminished lung capacity, her right lung was seen to function quite well following surgery.

Following her postoperative course of radiation therapy Arlene Berry remained quite well until about one week prior to her admission to the Kirkland and District Hospital on the 23rd of May 2000. Over that week she developed headaches that had become increasingly severe. A severe headache is a common but not invariable accompaniment of intracranial causes of nausea. In the last day or two she tended pulling to the right when walking, a sign of toxic ataxia, or ischemic limb from interruption of the blood supply to the spinal cord for example and for the two-week period prior to her hospital admission her headaches were accompanied by nausea , vomiting, and drowsiness, and were thought to be associated with a bout of the flu.

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 CIPRO, an antibiotic used for treatment of UTI (urinary tract infection), also indicated in the treatment of a variety of infections including influenza. The same record documents “blood when voiding”, that she was on antibiotics for 1 week and that she was given CIPRO, “1 given now”. The same record also documents nurses’ observations of “large blood trace leukocytes”. The same physician (whose signature is illegible) made a notation with respect to the flu, which was directed to the attention of the patient’s family MD (Dr. Jordan). From this record, it is clear that the physician who saw her made made a diagnosis of UTI. The test result from that diagnosis, WHAT I assume to have been a urine culture test seen at OP-55 of the outpatient record later returned a finding of “NO GROWTH” (a negative urine culture may suggest the presence of unusual bacteria or viruses causing symptoms of UTI). Compare gram-negative hematuria (pseudomonas aeruginosa, a gram-negative motilebacillus, is an opportunistic pathogen that frequently causes hospital-acquired infections). The same physician failed to consider her most recent treatments consisting of “radiation” and chemotherapies. He noted however that her recent head CT showed “NO METASTASIS” and that her mediastinoscopy that had been done at the same time also proved NEGATIVE. From that record it is clear that NO clinically detectable metastasis (the process by which tumors are spread) or mediastinal changes were found.

The outpatient record at OP-53 documents that she was pale-looking and lethargic.

What I take to be the health management record from the Kirkland and District Hospital at A-21 of the medical record documents that her cognitive perceptual pattern was seen as “sedated”, a sign of acute or late toxicity. The same record is totally devoid of annotation with respect to the patient’s bowel routine and elimination pattern for toileting marked by a complete absence of nursing care plan as further evidenced at A-21 of the medical record.

Further, what I take to be a continuation of the same record at A-23 documents that her speech was observed to be “slurred”, also a sign of toxicity.

The record at OP-54 dated May 22nd of 2000 documents a “haggard” appearance including “large blood trace leukocytes”. White blood cells (leukocytes) are elevated with dehydration, hyperviscosity secondary to dehydration, and infection.

The same record documents a question mark (?) with respect to possible morphine allergies, and that for 2 weeks she had the flu.

The same record documents bloody bowel movements for 4 days, including a history of morphine (MS Contin), Tylenol(acetaminophen), Aspirin and Demerol use.

Notably, the record does not take into account other medications prescribed or administered by the patient’s oncologist between March and the end of April of 2000. Compare Acetaminophen Toxicity.

From those records it is clear that Arlene Berry had a history of opiate use, among other medications and it was also noted that she had stopped taking the morphine for about a week. There is nothing on the record to suggest that the patient was ever tested or examined for possible side effects associated with the drugs she had been prescribed, or possible side effects such as associated with the withdrawal from opiates. Compare Morphine/Side Effects.

According to her family she had stopped taking the morphine due to increasing severity of constipation requiring extra laxative and tap water douches at home to assist with stool evacuation and also due to dizziness marked by a sense of uneasiness progressing to unsteadiness (lack of motorcoordination) and inappropriate behaviour as evidenced by family and friends.

A-12 of the medical record documents a list of what I take to be doctor ordered medications dated May 23rd of 2000. A-5documents the presenting complaint as headaches, accompanied by severe stomache pain (Abdominal Pain) ongoing for 2 weeks for which she was prescribed antibiotics. The RN who saw her noted that she had been taking MS Contin (morphine) for pain and that she had stopped taking the morphine, also noting her past medical history consisting of taking radiation. There is nothing on the record to suggest that she had been examined for the stomach pain either for constipation or possible bowel blockage associated with the morphine. Stomach pain is also a prominent finding associated with dehydration including constipation. Notably constipation, fecal impaction and bowel obstruction are common problems for oncology patients.

According to Dr. Jordan “she had presented to the ED (emergency department) several days before with vomiting and it was thought that she had a UTI”, to rule out delay in seeking treatment. He goes on to state that “she was given antibiotics and sent home” as evidenced at A-8.

According to the record she returned to the ED 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 seen at A-6.

What I also take to be a referral at A-6 of the medical record, a chart copy from the admitting physician directed to the attention of the attending physician documents what I take to be a provisional diagnosis of “vomiting”. Submit that vomiting is not a diagnosis but rather a symptom, or sign of many causes. A question was also raised with respect to possible metastatic CA of the brain leaving the etiology of the vomiting and the stomach pain left undetermined for the attention of the patient’s family MD. From that record it is clear that neither diagnosis nor differential diagnosis was made at that time, as evidenced by the record at A-3 and from that record it is also clear that nothing was entered because nothing was done.Further submit that abdominal pain concurrent with nausea and vomiting points to the abdomen as the source of the vomiting.

N-10 of the nurses’ notes document the patient’s level of care as “routine”. What I take to be a continuation of the same record at N-11 documents a diagnosis of “vomiting, lung CA”. There are no further entries on that two page assessment.

From the outpatient records alone it seems clear that there was every indication that Arlene Berry was about to suffer a catastrophic decline at least from foreseeable dehydration due to decreased oral intake and excessive vomiting over the previous week or more which ought to have prompted immediate medical attention. Other prominent signs and symptoms present prior to and at the time of her admission include fatigue, pale skin and blood tinged urine.

Dr. Jordan’s discharge note at A-1 documents that she was “afebrile” (without fever). In the upper right hand corner of the same report he documents anorexia, joint pain, and Urinary tract infection, 599.7 , using hand scripted numerical notations from the ICD (international classification of disease) code; i.e. 784.0 Anorexia, 787.3 Pain in joint , and 599.7 Urinary tract infection, site not specified 599.7 , respectively. The same report documents “plantars upgoing bilaterally”. Submit that upgoing plantar responses is a typical symptom of hepatic encephalopathy. The same record documents “ I was called in later that night because she had become obtunded”, while N-6 of the nursing notes documents “no response to verbal or physical stimulation” (obtundation) as early as 0030 hours on May 23rd of 2000.

According to the record at A-5 document that Dr. Jordan was notified at 0225 hours on May 24th. The same record documents Dr. Jordan’s no change in orders at 0100 hours, and in fact he did not show up until 0305 hours on May 24th as evidenced by the record at N-4 of the nurses' notes.

At the time of her admission to the hospital her BP (blood pressure) was documented at 115/70, with a pulse of 79 and regular, a respiration rate of 18, showing signs of mild diffuse (widespread) weakness as evidenced by the record at A-6 She was found to be alert and oriented with NO focal deficits.

Arlene Berry was admitted to the Kirkland and District Hospital on May 23rd of 2000 at 1845 hours whereupon she complained of being “cold”. She had the chills and so the nurses provided her with extra blankets. She was not very communicative due to extreme somnolence and stated that she was “very tired” (fatigue).

The same record at N-6 documents family in at 1915 hours and there is also a notation with respect to “emesis of ^ 100cc yellowish fluid”. (Note: when RBC's (red blood cells) complete their life cycle and break down naturally in the body they produce a “yellow pigment” which is then passed to the liver and excreted into bile).

She was still neurologically responsive when I saw here following her admission and in fact was able to reach and use for herself the kidney basin at her bedside table as she occasioned to vomit more of the flu-like “yellowish” bile that she had done so many times on the days before, and in fact used it for herself in our presence at which time a cool cloth was provided by the nurses. The same record documents that the patient stated that she was then “feeling a little better”. She was then assisted to bed. From that record it seems clear that she was at least benefiting from rehydration.

The medical record at N-6 documents telephone orders received by the hospital from Dr. Jordan at 2030 hours for “control of nausea”, for Stemetil” (prochlorperazine) 10mg. by “IV 4 times daily, given by the RN as evidenced by the physician’s orders at A-11 . Notable, prochlorperazine (Stemetil) is a high-risk antipsychotic-antiemetic drug to be used with caution according to manufacture’s directives. A typical single doses of Stemetil for a small woman with low body weight is 5 mg. From these records it is clear that Dr. Jordan elected to alienate and treat his patient unseen (at arm’s length), over the telephone and without first reviewing the patient’s files.

According to my information the duty placed on the doctor is to exercise care in all that is done to and for the patient which includes attendance, diagnosis, referral, treatment and instruction and its also clear that this was not done as further evidenced by the record at A-3 and the record as a whole. Further, there is nothing on the record which might explain the sudden absence of the severe stomach pain documented at A-5 of the nurse’s triage flow sheet signed by the RN.

The record at 0020 hours seen at N-6 documents the patient’s discovery by duty nurses of the patient’s “head against the left side bed rail with her feet under the right side rail” and without response to either verbal or physical stimulation and “dilated pupils” (a sign of possible overdosage, or decerberate (abnormal)posturing, with BP (blood pressure) rising. The admitting physician Dr. Spiller was up to assess the patient’s condition. Upon examination her eyes were documented as being sluggish noting also that there was no response to “deep pain”. She was simply repositioned by the nurses as evidenced by the record at N-6. From that record it seems clear that the patient had suffered a near fatal reaction to the given medication and that far from getting better she was becoming progressively worse as evidenced by a sense of urgency seen on the record to the attendance of the patient with increased activity documented at N-6 between 0030 and 0055 hours, as seen at N-5. Further, I assume that Dr. Jordan would have been alerted. He called in at 0100 hours but nevertheless opted not to change his orders as evidenced by the “no change in orders” also seen at N-5. that between 0200 and 0220 hours her BP had risen from 150/72 to 162/80, a sign of mounting hypertension, such as caused by a response to medications. The same record documents a heart rate (HR) in the 160’s with a rapid drop in blood pressure to 98/70 by 0235 hours.

From that record it seems clear that both doctors should have realized that they were faced with a critically ill young woman who was not responding to treatment and they should have been acutely aware of the danger. It is also of interest to note that no attempt was made by either of the doctors to place the patient in the ICU at that time (between 0030 and 0055 hours).

Further, N-5 of the record documents “family in” at 0250 hours. On seeing the patient, she was seen to be propped up in the arms of two nurses, gasping for air with only a plastic oral airway in her mouth. By 0220 hours the patient’s respiration rate was documented as “deep and soaring and without constant jaw thrust”, a sign of constriction.

The same record at N-5 document “gurgly” respiration’s that is consistent with swallowing difficulty suggestive of adversities to the given medication. Also, the same record documents a rapid drop in blood pressure to 98/70 at 0235 hours with physician “assessments unchanged” despite the fact that the patient had already gone into respiratory distress as evidenced by “Cheyne-Stokes” respirations with periods of apnea lasting 5-8 seconds. Notably, the central mechanisms that regulate breathing fail in severe hypoxia leading to irregular respirations, Cheyne-Stokes breathing, apnea, and respiratory cardiac failure (hypoxia leads to obtundation). Notably, there is nothing on record to suggest that the patient was oxygenated prior to intubation and from these records it is clear that the health care providers withheld life support when the patient became critically ill.

The same record at 0255 hours documents a “sudden large bloody emesis of reddish brown” what is known in medical circles as “coffee-ground vomitus” (dark brown vomitus the colour and consistency of coffee-grounds composed of gastric juices and old blood) indicative of a slow bleeding source in the upper GI tract. Notably multiple medications, restricted diet or poor nutrition causes gastrical intestinal (GI) lesions to GI bleeding. Further, GI bleeding is considered a potential medical emergency. From that record, it is clear that nothing was immediately done to determine a possible cause or treat accordingly and that Dr. Jordan showed no concern for this patient is spite of her worsened condition. Also, Dr. Spiller (the ED physician) did nothing to lessen or prevent the outcome, suggestive of his complicity or acquiescence to test the efficacy of the given drug (Stemetil) or outright incompetence or other negligence.

The record at N-4 documents the patient’s “transfer to ICU” at 0320 hours. The record at A-27 documents a blood pressure of 163/117 at the very same time. The presence of severe elevation of blood pressure with a diastolic blood pressure greater than 120mm Hg is considered a hypertensive urgency that requires reduction.

The record at A-24 documents the 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, that no attempt was made by the healthcare providers to place the patient in the ICU prior to 0320 hours and further that the patient’s condition remained critical throughout the night and into the small hours of the morning notwithstanding. The same record documents a heart rate (HR) of 174 bpm at 0320 hours that is consistent with trauma.

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

The record at N-4 documents “incontinent blood tinged urine” at 0305 hours that is consistent with hematuria and ‘large blood trace leukocytes” documented at OP-54, while N-3 of the record documents a ‘large amount of dilute urine’ at 0325 hours, only 20 minutes later and again at 0450 hours as documented at N-1 that is inconsistent with the record as a whole and in particular with respect to A-16 marked by a complete absence of documentation as to water refill as to justify urine output, evidenced by the complete absence of documentation for “elimination” seen at N-10 of the record.

There are numerous material deficiencies in the related medical records in which several pages of documentation manifest a lack of internal consistency ranging from out of sequence reports such as the triage record seen at A-5, to obviously rewritten, altered and falsified nursing notes seen at N-1, N-2 and N-3, marked by error, inconsistency and contradiction, to the ventilation record seen at A-16 and A-17 presenting similarly.

The physicians diagnostic sheet at A-3 ought to have been placed on the record at the time of the patient’s admission as well as the emergency record seen at A-4 . Notably, both of these records were dated using a rubber stamp.

Further, the ambulance call report was filed on the record at N-7 and N-8 of the nursing notes. That document ought to have been placed on the patient’s file on or about the time of the patient’s discharge.

The record at A-6 documents the patient as having a history of metastatic lung cancer, while the record at OP-54 documents “NO MESTASIS”, and medianastoscopy “NEGATIVE”.

There are several late dictations, all of them questionable and I can count at least 3 in all seen at A-1 and A-2, also A-6 and A-7 and also at A-8 and A-9 of the medical records as evidenced by the times and dates upon which they were dictated and transcribed. Other evidence may present upon forensic examination.

A-1 of the record documents “she had a left lung pneumonectomy back in October of 1999", which is erroneous. The same record documents “I was called in to see her later that night because she had become obtunded”. Notably, neuroleptic drugs, i.e., phenothiazines, including prochlorperazine (Stemetil) can also lead to coma/obtudation. A-17 documents “removal of left lung in ‘99”, the very same error, suggestive of having been copied.

A-1 of the record also documents “she died several days later with numerous metastatic lesions to her brain” which is also erroneous. Arlene Berry died May 24th of 2000 the very same day as evidenced by her death certificate. As to the cause of death the facts speak for themselves.

What I take to be the ventilation record at A-17 documents the arrival of Helene Studholme (ventilatory therapist) in the ICU at 0330 hours after being “called in for patient requiring ventilation”. N-3 of the record documents the time of the patient’s intubation by Dr. Jordan at 0325 hours, 5 minutes earlier. The same record documents patient “suctioned down ET tube several times for small amount of brownish mucous” while A-17 documents “being suctioned for moderate amounts of coffee-ground emesis by RN” at 0330 hours that is consistent with GI (gastrointestinal) bleeding.

N-2 of the record documents the ET (endotrachial tube) “pulled back” at 0425 hours, the patient having been intubated at 0325 hours. From that record it is also clear that the ET (endotrachial tube) had been malpositioned one full hour before the error was discovered by one of the nurses, as evidenced by that record. Both myself and the patient’s foster brother were present to witness that event.

According to my research “when an endotrachial tube is misplaced in the esophagus and misplacement is detected late, the compromise of the patient’s safety can be significant. (Perforation of a viscous into the peritoneal cavity, i.e. the intra-abdominal esophagus, or other trauma related causes in which ascites may become infected secondary resulting in spontaneous bacterial peritonitis cannot be ruled out).REFERENCE. A-26 of the record documents a BP of 78/70 at 0235 hours while N-5 documents BP of 98/70 at the very same time that is consistent with copious error.

A-16 documents a BP of 163/117 at 0330 hours, while N-3 documents a BP of 136/85 at the very same time.

At 0352 hours the patient’s blood pressure was documented at 85/52, some 17 minutes later, as evidenced at N-2 (in which blood pressure is inadequate for normal perfusion and oxygenation, to rule out prompt replacement of blood and fluid volumes). According to my investigation, at the point of loss of blood pressure the resulting end organ injury is often irreversible i.e., endothelium, lung, kidney, liver, etc.

A-24 of the record documents a heart rate (HR) of 154 at 0330 hours, while the Ventilation Record at A-16 documents at HR of 126 at the very same time, a significant difference.

From these records it is clear that nothing was done to bring the patient’s BP under control in a timely manner and would have resulted in permanent brain damage at that point. According to my research, there would have been a loss of perfusion and autoregulation with the rapid drop in BP and it is also clear that nothing was immediately done to correct it. It is interesting to note that adequate cerebral perfusion must be restored within 3-5 minutes for complete neurological recovery.

The physician’s critical care note, a late dictation which purports to have been dictated at 0420 hours on May 24th of 2000 seen at A-8 of the record documents “later that evening she rapidly deteriorated and became unconscious without responding to verbal stimuli or painful stimuli”, while the record at N-2 of the nursing notes documents “attempts to pull away to painful stimuli” at 0400 hours only 20 minutes earlier.

(Note: I had asked the patient in the presence of her foster brother, if she could hear me to wiggle her toes and she did, not once but twice. In my opinion, she appeared to be more paralyzed than anything).

A-16 of the record was initialled by both Helene Studholme and Janice Chamaillard. The latter is the author of N-1 through N-3 of the record, and the co-author of A-16 while 75% of the ventilation record was authored by helene Studholme. The two versions of the patient’s vital signs is proof of deception, and fabrication on the part of healthcare providers.

What I take to be the physician’s lab record at A-17 and A-25 documents the patient’s vital signs at 5 minute intervals, beginning at 3:15 hours. There is a complete absence of record in several distinct columns, primarily relating to the patient’s vital signs at the time of the intubation procedure, suggestive of edited lab notes by the physician after the fact to conceal iatrogenic (doctor caused) injury. Notably, what I take to form a part of a continuous two page record appear to have been printed on two separate printers. Ironically, both pages are marked Page 1 of 1 (in lieu of Page 1 of 2, and 2 of 2), to rule out conformity or consistency. Further, when both pages are overlapped and held over a light, the printed headings are misalligned, and the print sizes are slightly different.

The Cardiac Index at A-18 documents the patient’s vent rate at129 bpm at 0417 hours with heart and breath rate increased, Sinus Tachycardia that is consistent with systemic inflammatory response to clinical insult such as caused or worsened by medications suggestive of Neuroleptic Malignant Syndrome (NMS). Pathologic tachycardia accompanies with anoxia (lack of oxygen to tissues) as caused by anemia, congestive heart failure, hemorrhage or shock. The same report documents an inferior ischemia (decreased blood supply to vital organs) suggestive of arterial occlusion , which can induce cerebral tissue ischemic injury by producing mid-line shift and herniation resulting in reduced blood flow. The same document shows an abnormal ST&T wave segment on ECG that is consistent with adverse effects of the given drug Stemetil. Also, the patient’s age was falsely documented at 55 years (she was only 41 years of age).

The physician’s lab work summary at A-19 documents the charting of a course of hematologyand blood coagulationtherapy. It documents a FIBRINOGEN level of 4.67 H (normal 2.00-4.00), increased in response to injury,hypotension, and trauma, and a D-dimer test level of 1000 H (<500), including hematological findings in the High (H) and Low (L) ranges, suggestive of pathology associated with a hematologic disorder. According to my research, high levels of fibrinogen can cause abnormal arterial blood clotting. Serum fibrinogen levels in a safe range is <300 mg/dL. Fibrinogen acts to promote platelet aggregation (clumping together of platelets at the site of injury) resulting in diminished blood flow and delivery of oxygen to the body, i.e. arteries, heart, and brain. D-dimer suggests thrombosis (blood clotting) and is the confirmatory test in DIC (disseminated intravascular coagulation).

The aPTT (coagulation partial thromboplastin time) a test used to determine the efficacy of various clotting factors used in the diagnosis of blood coagulation disorders documents the therapeutic range for Heparin therapy at 60-100 seconds (23-35 is the normal) and is elevated in 90% of those with coagulopathy, an increased bleeding tendency due to decreased hepatic synthesis of clotting factor, i.e. with prothrombin ( a protein involved in blood clotting) time increased. The time of that assessment was documented at 0400 hours. Compare DIC (disseminated intravascular coagulation).

The same record documents the patient’s blood cell count beginning with the WBC's White blood Cell (leukocyte) count of 22.4 #PH (normal 4.0-11.0), increased to more than double the normal range with allergic response to 22.4 H. White blood cells (leukocytes) are elevated with dehydration, hyperviscosity secondary to dehydration and infection causes. It is the most common form of leukocytosis, to rule out benign white cell disorder.

The record at A-19 documents a Lymphocyte Count of 2.0 L (low) suggestive of lymphocytopenia in which lymphocytes are reduced with nutritional deficiency, infection or an exhausted immune system. Lymphocytopenia causes may arise from accelerated destruction of T cells or other syndromes associated with depletion of blood lymphocytes. Interestingly, iatrogenic lymphocytopenia is caused by cytotoxicchemotherapy and radiation therapy, marked by a reduction in the absolute number of T cells (lymphocytes are the most sensitive to whole body radiation and their count is the first to fall in radiation sickness).

The same record documents an Absolute Lymph’s (Lymphocyte)Count of 0.4L (low), suggestive of fluid build-up in the abdomen ( ascites ) in which liver disease is the most common cause. If the ascites is due to liver disease the fluid may be clear to “yellowish”, uninfected and have a low cell count. If bacterial infection is present in ascites this may suggest spontaneous bacterial peritonitis in which abdominal pain is a prominent finding. (If peritonitis is not treated promptly and effectively multisystem organ failure occurs rapidly).

Further, the same report documents Neutrophils (also known as granulocytes) with a count of 92.0 H (normal 47.0-77.0) shows absolute Neut’s of 20.0 H (normal 1.3-6.7) increased in response to acute infections (bacterial or viral), drug toxicity and hemorrhage.

The HCT (hematocrit) shows a count of 0.361 L (low). Hematocrit is the measurement of the percentage of red blood cells in whole blood with a reduction suggestive of anemia. Normal Adult Female Range is 37-47%. Anemia is present when hematocrit is <37% in women.

The RDW ( Red Cell Distribution Width) shows a count of 18.4 H (normal 11.50-16.8) increases before MCV (Mean Corpuscular Volume) becomes abnormal suggestive of anemic globinopathy. Its principal function is to transport oxygen and becomes elevated with oxygen deprivation, as to infer inadequate oxygenation.

Also, the same report documents a Platelet Count of 544 H increased with coagulopathy (platelet coagulant activities) or platelet aggregation (cohesion of platelets to each other forming clumps). Platelets (also known as thrombocytes) coagulate the blood. Platelets plug bleeding capillaries and vessels. With infection or injury, white blood cells rush to the site as the first line of defense. Platelet aggregation contributes to the coagulation cascade with activation, i.e. esophageal perforation or other trauma/procedures and can lead to DIC and hemorrhage. In addition to drug reactions, platelets are elevated with dehydration. Larger platelet volume also indicates younger and more active platelets of recent onset volume (equivalent of MCV for red cells) in the complete blood count (CBC) report.

The same record documents Absolute Mono’s (monocytes) with a count of 0.60 (normal 1.0-5.5) with a reduction indicative of a state of health. Monocytes are considered the body’s second line of defense against infection. In carcinoma (cancer) or leukemia, the moncytes become “elevated”, to rule out metastasis. Toxic substances can also injure monocytes.

A-20 of the laboratory discharge summary documents a serum potassium level of 3.4 L (hypokalemia ) as caused by ongoing or severe fluid losses form the GI tract, i.e., such as from vomiting and malnutrition which can lead to weakness, fatigue and cardiac problems. Anything below 3.5 creates a serious risk of cardiac arrhythmia leading to cardiac arrest. No potassium replacement was ordered or administered. It is not known what the patient’s potassium level was at the time of her admission. No lab tests were performed soon enough to verify or treat accordingly. In my opinion the ED physician should have ordered monitoring by electrocardiogram and done appropriate testing at the onset, but failed to do so.

A-20 of the record documents an Arterial pO2 (blood gasses) of 129.0 H (normal 75-100) increased in respiratory alkalosis, metabolic alkalosis, drug overdosage and cardiac arrest. The PaO2 (partial pressure of oxygen) increases with hyperventilation leading to hyperacidosis and hypercalmia.

The same record documents an O2 Saturation of 98.9 H. Pulse oximetry estimates the O2 saturation of the hemoglobin. (Normal is 93 – 97%.) Abnormal results may indicate respiratory, metabolic, or renal diseases. Results may also be abnormal in trauma, particularly with head or neck injuries that may affect breathing, and has also been has been associated with incubation phase of acute hepatitis, 5 week (mean 28 days) with asymptomatic infections common, and also correlates with the cirrhotic stage of liver disease.

The ambulance call report seen at N-7 of the nursing notes documents that the patient was intubated and vented and that she was seen to be stable but that she appeared to be “pale, dry and cool” (clinical manifestations of adrenal insufficiency). There is an X mark in the box pertaining to allergies NKA suggestive of NO KNOWN ALLERGIES, and a further notation claiming “Dr. now suspects that cancer has gone to the brain”. The same report documents “intacramial bleed” that is inconsistent with the “coffee-ground emesis” documented in the nursing notes and on the ventilation record on or about the time that the patient was intubated. The same report also documents “pulses x 4 good”, including head/neck OK; chest OK; abdomen OK; pelvis OK; and extremities OK. The very same report documents a Nature Code 0 (No Code = No Care), a withdrawal of life support from a critically ill patient or DNR (do not resuscitate order, issued against family wishes. The time of that report was documented at 0620 hours on May 24th of 2000, only hours before the patient’s death.

According to the nursing notes at N-1 of the record the patient was given Gravol 50 mg 10 by paramedics at 0620 hours, while the record at N-7 with respect to medications documents “See Nsg Notes”. Notably, Dimenhydrinate (Gravol®) is contraindicated in chronic lung disease and has also been reported to mask the toxic effects of other drugs.

ADDITIONAL READING:

Radiation Injury Of The Nervous System
CNS Paraneoplastic Syndromes
Signs & Symptoms
Online Health Analysis: Conditions: Hepatitis
The Merk Manual of Medical Information
The Merk Manual of Diagnosis and Therapy
The Merk Manual of Geriatrics
Diseases of the Liver
Hepatic encephalopathy
CLINICAL FEATURES OF HEPATIC ENCEPHALOPATHY
COMMON PRECIPITANTS OF HEPATIC ENCEPHALOPATHY
GLOSSARY FOR PERFUSION TECHNOLOGY
Hepatic Encephalopathy DEFINITION:
Precipitating Factors:
Hepatic encephalopathy: Treament Toxic/Metabolic Disorders
What Are The Main Symptoms Of Hepatitis C
MEDICAL ISSUES
RESPIRATION
KEYWORDS
BLOOD GASSES
BLOOD GASSES, ELECTROLYTES,
ARDS
Factors that Influence Oxygenation
Oxygen Toxicity
Acute Respiratory Failure
IDENTIFYING MEDICAL MALPRACTICE
THE JKL MEDICAL DICTIONARY
H: (H. influenzae- Hemoglobinopathy)
Interpretation of Lab Test Profiles
LABORATORY TESTS
LABORATORY TRAINING MANUAL
Symptoms of Hepatitis
LABORATORY TESTS
Hep-C Awareness Project
Treatment
The Infections
FATIGUE
MEDICAL ERRORS & ADVERSE DRUG REACTIONS
Iatrogenic Illness
HEMATOLOGY
Oncologic Pathology Internet Resources
ONCOLOGIC EMERGENCIES
ONCOLOGIC EMERGENCIES
Radiation Damage
Conditions with Similar Symptoms as: Radiation Damage
RADIATION EMERGENCIES
Acute Radiation Syndrome
ACUTE RADIATION SYNDROMES
NUTRITION
Blood in the Stool
Bedside Logic in Diagnostic Gastroenterology
Nausea and Vomiting
The ABC's of hepatitis
Fatigue
Infectious diseases - hepatitis
Introduction to Acid-Base Balance and Arterial Blood Gas Analysis
Normal arterial blood pressures with age
Normal electrolyte concentrations in blood
Average haematological values
Normal arterial blood pressures with age
Common medical and biophysical abbreviations
Typical single doses of Prochlorperazine Stemetil= 5 mg
PaO2, SaO2 and Oxygen Content
All You Really Need to Know to Interpret Arterial Blood Gases
All You Really Need to Know to Interpret Arterial Blood Gases
All You Really Need to Know to Interpret Arterial Blood Gases
Additional Arterial Blood Gas Resources
Chemistry and Lab Management Links
Arterial Blood Gas (ABG) Basic Tutorial
lab Tests Online
Lab Tests - Normal Values
How Reliable is Laboratory Testing?
INTRODUCTION TO LABORATORY MEDICINE CLINICAL PATHOLOGY
Introduction to Laboratory Testing
Lab Tests Online
Lab tests online
Lab Tests
Complete Blood Cell count (CBC)
LAB TESTS
Viral Hepatitis
Interpretation of Lab Test Profiles
LAB
Arlene Berry
DEATH CERTIFICATE