Thunder Bay Independent Media Center -------------------------------------------------------------------------------- Original article is at http://thunderbay.indymedia.org/news/2002/08/1274.php kdhospitalscandal by Malcolm Everett • Wednesday August 28, 2002 at 12:07 PM meverett@prweb.com KIRKLAND LAKE, ON The Kirkland and District Hospital Coverup Continues The Arlene Berry Case:

Update

INVESTIGATIVE REPORT

The Arlene Berry Case

RE: Arlene H Berry

Date of Death: May 24, 2000

Arlene H. 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, i.e. liver encephalopathy, or toxic hepatitis. She was transferred to Sudbury Regional Hospital only hours before she died. No autopsy was performed.

FOREWARD

Submit that predisposing factors in hepatic encephalopathy include a history of blood in urine or stool, opiate use, infection, GI bleeding, dehydration or electrolyte abnormalities. Compare liver encephalopathy. http://www.principalhealthnews.com/topic/topic100587091

Hepatic encephalopathy (HE) is a syndrome of impaired brain function due to liver failure. Iatrogenic HE thus describes a part of this syndrome which is precipitated or worsened by medical procedures or treatments v 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. http://www.merck.com/pubs/mmanual/section4/chapter38/38f.htm Drug-induced hepatitis http://health.yahoo.com/health/dc/000226/0.html Drug-Induced Hepatitis http://www.sw.org/clinical_content/adult/liver/drughep.htm

Submit that predisposing factors in hepatic encephalopathy include a history of blood in urine or stool, opiate use, infection, GI bleeding, dehydration or electrolyte abnormalities. Compare liver encephalopathy

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. Compare portal systemic encephalopathy. http://www.merck.com/pubs/mmanual/section4/chapter38/38f.htm

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. http://www.hepnet.com/liver/disease.html 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. http://www.emedicine.com/med/topic1184.htm

Also, patients with hepatitis C can have normal liver enzyme, and still have liver disease. Compare “compensated cirrhosis” in which patient’s with early stage cirrhosis may not have any symptoms or laboratory test abnormalities. http://www.medhelp.org/forums/Hepatitis/messages/C32616-4.html

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. Medication effects and other systemic diseases as causes mandate a thorough drug history. Ref: http://www.merck.com/pubs/mmanual/section4/chapter43/43d.htm

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 the medical record of Arlene Berry for May 23rd and

These are the facts

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 (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. 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 at OP-54documents 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 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 motile bacillus, 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 MESTASIS” and that her medianastoscopy that had been done at the same time also proved “NEGATIVE”. From that record it is clear that NO clinically detectable mestasis (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 and

What I take to be the health management record from the Kirkland and District Hospital at A-21of 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 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-54dated May 22nd of 2000 documents a “haggard” appearance including “large blood trace leukocytes”. White blood cells (leukocytes) are elevated with dehydration, hyper viscosity secondary to dehydration, and infection. The same record documents a question mark (?) with respect to possible morphine allergies. Compare side effects of cancer treatments. for 2 weeks had the flu.

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

From these 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 motor coordination) 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 stomach 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 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 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 of many causes. A question was also raised with respect to possible mestastatic 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.

N-10of 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 hematuria using hand scripted numerical notations from the ICD (international classification of disease) code; 784.0, 787.03, and 599.7 respectively. The same report documents “plantars upgoing bilaterally”. Submit that upgoing plantar responses is a prominent finding in hepatic encephalopathy. The same record documents “ I was called in later that night because she had become obtunded”, while N-6of 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. At the time of her admission to the hospital her BP (blood pressure) at A-6of the record was documented at 115/70, with a pulse of 79 and regular, a respiration rate of 18 and signs of mild diffuse (widespread) weakness as further 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 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. IV bid prn (twice daily) by IV 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. 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. (Note: 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-6documents 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 overdosage) with 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 atN-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 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).

N-5of 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 atN-5document “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-4documents 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-4Notably, both of these records were dated using a rubber stamp.

Further, the ambulance call report was filed on the record at N-7and 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-2of 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). Ref: http://www.emedicine.com/EMERG/topic176.htm http://www.emedicine.com/emerg/byname/esophageal-perforation-rupture-and-tears.htm

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-16documents 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-8of 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).

A16 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-16while 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 atA-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-18documents 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 NMS (neuroleptic malignant syndrome). Pathologic tachycardia accompanies anoxia (lack of oxygen to tissues) as caused by anemia, congestive heart failure, hemorrhage or shock. The same report documents an inferior ischemia (decreased blood supply to vital organs) suggestive of intracranial hypertension, which can induce cerebral tissue ischemic injury by producing mid-line shift and herniation resulting in reduced blood flow. The same document shows ST&T wave abnormalities and abnormal 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 hematology and blood coagulation. 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 level of 1000 H (<500), including hematological findings in the High (H) and Low (L) ranges. 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 disseminated intravascular coagulation (DIC).

The aPPT (activated partial prothrombin 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 (white blood cell) 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, hyper viscosity secondary to dehydration and infection causes. It is the most common form of leukocytosis. Compare 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 cytotoxic chemotherapy 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 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 mestasis. 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. This level has 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 dehydration and shock). There is an X mark in the box pertaining to allergies NKA suggestive of allergies unknown 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, 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 atN-1of 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, Gravol is contraindicated in chronic lung disease and has also been reported to mask the toxic effects of other drugs.

SOURCES/REFERENCES

Drug-Induced Liver Diseasehttp://www.courses.ahc.umn.edu/pharmacy/5880/Lecture_Outline/hepatic_disease.htm

General Symptoms Related To Gastrointestinal Disordersvhttp://www.intelihealth.com/IH/ihtIH/WSIHW000/8270/8528/189144.html?d=dmtContent

Drug Induced Disordershttp://www.aafp.org/afp/971101ap/holland.html

Common Electrolyte Disturbances in the ED http://enw.org/Electrolytes.htm

Hypokalemia http://www.emedicine.com/emerg/topic273.htm

Hyperkalemia http://www.emedicine.com/emerg/topic275.htm

Recommendations for the Use of Antiemetics: Evidence-Based, Clinical Practice Guidelines – American Society of Clinical Oncology Special Article

http://208.243.117.239/prof/pp/html/guide/anti/antiem.pdf

White Cell Disorders: Leukocytosis Http://hsc.virginia.edu/medicine/clinical/pathology/educ/innes/text/wcd/leukocytosis.htm

Leukocytosis http://cpmcnet.columbia.edu:70/mdxdocs/ddl47.htm

P-I-E-N-O Parkinsn’s List Drug Database

http://www.parkinsons-information-exchange-network-online.com/ http://www.parkinsons-information-exchange-network-online.com/drugdb/108.html vhttp://www.parkinsons-information-exchange-network-online.com/drugdb/drugdb.html http://www.parkinsons-information-exchange-network-online.com/

http://www.parkinsons-information-exchange-network-online.com/drugdb/sitemap/ http://208.243.117.239/prof/pp/html/guide/anti/antiem.pdf

Acute Diseases Of The Liver http://blue.vm.temple.edu/~pathphys/gi/acute_liver.html Neurological Pathophysiology: Hypoxia

Radiation Necrosis from Neurology/Neuro-oncology http://www.emedicine.com/neuro/topic330.htm

Benign Intracranial Hypertension http://www.ihrfoundation.org/about-ih/default.asp NINDS Pseudotumor Cerebri Information Page Synonym(s): Benign Intracranial Hypertension, Intracranial Hypertension

http://www.ninds.nih.gov/health_and_medical/disorders/pseudotumorcerebri_doc.htm

Benign Intracranial Hypertension (Pseudotumor Cerebri) http://www.merck.com/pubs/mmanual/section14/chapter177/177c.htm

Thrombosis Online http://www.thrombosis-online.net/

HEPATIC ENCEPHALOPATHY http://www.medhelp.org/glossary/new/gls_2197.htm http://www.emedicine.com/med/topic3185.htm http://gastroresource.com/GITextbook/En/Chapter14/14-13.htm http://www.merck.com/pubs/mmanual/section4/chapter38/38f.htm http://hepatitis-central.com/hcv/symptoms/encephalopathy/subclinical.html http://www.hepnet.com/liver/disease.html

Common Laboratory Tests in Liver Diseases http://cpmcnet.columbia.edu/dept/gi/labtests.html

Toxic and Drug-Induced Hepatitis Clinical Resourceshttp://cchs-dl.slis.ua.edu/clinical/gastroenterology/hepatic/hepatic/hepatitis/toxichepatitis.htm

TOXIC HEPATITIS

http://www.liver.ca/english/liverdisease/toxic_hepatitis.html http://www.fpnotebook.com/GI70.htm http://hepatitis-central.com/hcv/hepatitis/toxic.html http://www.nlm.nih.gov/medlineplus/ency/article/000226.htm http://www.healthatoz.com/atoz/Hepatitis/hepres.html http://www.cag-acg.org/patinfo/toxic_hepatitis.htm

CANCER RADIATION THERAPY- Disease Therapies Protocol http://www.lef.org/protocols/prtcl-025.shtml

Gastrointestinal, Hepatic and Pancreatic Disorders/Management (GH) http://www.dal.ca/~pharmwww/pdiwdyfi/gi.htm

Vascular Mechanisms Of Central Nervous System Injury http://research.medicine.wustl.edu/ocfr/research.nsf/Abstracts/234B69C253C5936D8625677D00592CAF Open Document&VW=Inflammation (Search within this site) SGD: Increased Intracranial Pressure... http://www.ohsu.edu/som-Nsb/SGD/SGD.2.13.A-1000.html

NERVOUS SYSTEMhttp://pathcuric1.swmed.edu/PathDemo/cnsqs/cnsqs.htm

The Complete Neurological Examination http://www.medinfo.ufl.edu/year2/neuro/neuroexam/neuroexm.html

Opioid-induced nausea and vomiting http://www.nauseaandvomiting.co.uk/

Drug-induced hepatitis http://www.nlm.nih.gov/medlineplus/ency/article/000226.htm Supportive Care & Symptom Control Regimens http://www.cancercare.on.ca/formulary/supxcondition.html Nausea and Vommiting http://www.mdbrowse.com/Speciality/Family-prac/Nausea&Vommiting.htm e.g.- .Opiates, phenytoin, digitalis, salicylates, aminophylline, chemotherapy

Drug-induced Gastrointestinal Disorders

http://www.medscape.com/viewarticle/437034

Blood Cells and the CBC http://www.neosoft.com/~uthman/blood_cells.html

Activated Partial Thromboplastin Time (APTT) http://millenova.com/tests/aptt.asp Hemorrhagic disorders http://www.ecc.cc.mo.us/ecc/library/web/reserves/hemorrhagicdisorders.htm

FULL BLOOD COUNT (FBC)

http://www.rcpa.edu.au/pathman/full_blo.htm http://www.mydr.com.au/default.asp?article=3011 http://www.teaching-biomed.man.ac.uk/student_projects/2000/mnat7sr2/fullbloodcount.htm http://www.bggp.co.uk/presentations/The%20Full%20Blood%20Count/

What is a Full Blood Count? http://www.hibernianhealth.com/fullbloodcount.html

Disseminated Intravascular Coagulation http://www.emedicine.com/emerg/topic150.htm http://rnbob.tripod.com/dic.htm

DISORDERS OF BLOOD COAGULATION http://cpmcnet.columbia.edu/texts/guide/hmg23_0009.html

Definition for: DIC http://www.kumc.edu/instruction/medicine/pathology/ed/keywords/kw_dissemin1.html MEDLINEplus Medical Encyclopedia: DIC (disseminated intravascular http://www.nlm.nih.gov/medlineplus/ency/article/000573.htm

LIVER DISEASE-RELATED COAGULATION DISORDERS THE MERCK MANUAL, Sec, 11, CH, 131, hemostasis And Coagulation http://www.merck.com/pubs/mmanual/section11/chapter131/131d.ht

NB: This report represents approximately 4,000 man hours time expended to research and investigation into the unnecessary death of Arlene Berry and can be substantiated by evidence based medicine as published by leading authorities

LEGAL CONSIDERATIONS (**)

Submit, that “when a patient presents or is brought to emergency, the request for care should be presumed to be urgent”.

“The most common components of the doctors duty of care to a patient are the duty to attend, diagnose, refer, treat and instruct.”

“The duty to diagnose requires doctors to take a full history, use appropriate tests and consult or refer if necessary. They must take reasonable care to detect signs and symptoms and formulate a diagnosis using good judgement. They cannot act only on what they are told nor can they ignore what they are told.”

“The court then looks for evidence of considered medical judgement reflected in planning for the particular patient’s care and safety” .

** taken from the text “Legal Liability of Doctors and Hospitals in Canada,” by Picarde & Robertson, 3rd ed., Carswell-1996.

There are a number of related criminal offences which apply here, including criminal negligence causing death.

The Criminal Code defines criminal negligence as acting with wanton and reckless disregard for human life, the maximum penalty of which is life, and criminal negligence causing bodily harm, the maximum penalty of which is 10 years.

Causing death by criminal negligence

220. Every person who by criminal negligence causes death to another person is guilty of an indictable offence and liable (a) where a firearm is used in the commission of the offence, to imprisonment for life and to a minimum punishment of imprisonment for a term of four years; and (b) in any other case, to imprisonment for life. R.S., 1985, c. C-46, s. 220; 1995, c. 39, s. 141.

Causing bodily harm by criminal negligence

221. Every one who by criminal negligence causes bodily harm to another person is guilty of an indictable offence and liable to imprisonment for a term not exceeding ten years. R.S., c. C-34, s. 204.

Homicide

222. (1) A person commits homicide when, directly or indirectly, by any means, he causes the death of a human being.

Kinds of homicide (2) Homicide is culpable or not culpable.

Non culpable homicide (3) Homicide that is not culpable is not an offence.

Culpable homicide (4) Culpable homicide is murder or manslaughter or infanticide.

Idem (5) A person commits culpable homicide when he causes the death of a human being, (a) by means of an unlawful act; (b) by criminal negligence; (c) by causing that human being, by threats or fear of violence or by deception, to do anything that causes his death; or (d) by willfully frightening that human being, in the case of a child or sick person.

Exception (6) Notwithstanding anything in this section, a person does not commit homicide within the meaning of this Act by reason only that he causes the death of a human being by procuring, by false evidence, the conviction and death of that human being by sentence of the law. R.S., c. C-34, s. 205.

Acceleration of death

226. Where a person causes to a human being a bodily injury that results in death, he causes the death of that human being notwithstanding that the effect of the bodily injury is only to accelerate his death from a disease or disorder arising from some other cause. R.S., c. C-34, s. 209.

227. [Repealed, 1999, c. 5, s. 9] Accessory after the fact 23. (1) An accessory after the fact to an offence is one who, knowing that a person has been a party to the offence, receives, comforts or assists that person for the purpose of enabling that person to escape. (2) [Repealed, 2000, c. 12, s. 92] R.S., 1985, c. C-46, s. 23; 2000, c. 12, s. 92.

Criminal Code ( R.S. 1985, c. C-46 ) Disclaimer: These documents are not the official versions (more). Source: http://laws.justice.gc.ca/en/C-46/text.html Updated to August 31, 2001

The following is a recent case in which a doctor was convicted of criminal negligence:

R. V. MANJANATHA, (1994-11-04) SKCA CA94154 Saskatchewan >> Court of appeal >>

R. V. MANJANATHA, (1995-06-21) SKCA CA95081 /Source: http://www.canlii.org/sk/cas/skca/1994/1994skca94154.html Saskatchewan >> Court of appeal >> R. V. MANJANATHA, (1995-06-21) SKCA CA95081 http://www.canlii.org/sk/cas/skca/1995/1995skca95081.html

ARTICLES FRO IEEE ENGINEERING IN MEDICINE AND BIOLOGY http://biotech.law.lsu.edu/IEEE/ieee09a.htm

Criminal Code of Canada