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.

In December of 1999, Arlene Berry was sent to Timmins where she was diagnosed with carcinoma of the left main bronchus with residual CA (cancer) 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, also known as Dr.Claudio Alberto 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, i.e "bleeding" 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 known 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, lack of motor coordination, 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. Common side effects of Cipro include "nausea", followed by headache, restlessness, abdominal pain and bloating". 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 a "slurred speech”, 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. i.e. Senokot for constipation, side effects of which include "severe stomache pain", and unusual change in color of urine. She was also given Tylenol with Codein, including Amoxicillan for infection. Amoxicillan belongs to a class of drugs called penicillin side effects of which include "severe nausea and vomiting", including "abdominal pain". Additionally she was given Demerol. 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 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-5 documents 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  of the hospital record.

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 . The same record, what is Dr. Spiller's physical examination also documents a "soft, non-tender" abdomen, and "no masses". Submit that an enlarged liver usually feels soft due to liver enlargement (hepatomegaly), a sign of liver disease. It is also associated with hepatitis , fatty infiltration, congestion with blood, and early obstruction of the bile ducts. Distinct, on the other hand, suggest cancer. The record documents "no masses".

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. Indications are primarily in the management of psychotic disorders.Unexplained, sudden deaths have occurred in hospitalized patients treated with this drug.

According to my investigation, prochlorperazine is widely distributed into body tissues and crossed the blood-brain barrier. The drug is highly plasma protein bound (91-99%). The duration of activity is 4 to 6 hours. It is of particular interest to note that the drug undergoes metabolism in the gastric mucosa and on the first pass through the liver. Case reports include liver toxicity. A typical single dose 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 (BP) 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. Gastrointestinal bleeding should have been controlled if possible and blood purged from the gastrointestinal tract. Further, Dr. Spiller (the ED physician) did nothing to lessen or prevent the outcome, suggestive of his complicity or acquiescence to coverup Dr. Jordan's stupidity, 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  at N-9 ,   N-10,                                  N-11 , and  including  A-3  and A-21  of the medical record.

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.

Further,  N-3  documents a 'large amount of dilute urine' at 0330, and also at 0425 hours as evidenced by the record at  N-2, and again at 0450 hours as evidenced at  N-1,  suggestive of overly rapid fluid overload due to negligent overzealous  IV infusion.

 NOTE:  There is nothing on record to suggest close monitoring of serum sodium  (serum Na) levels.  Irreparable harm can befall a patient when abnormal serum sodium levels are administered or corrected too quickly or too slowly. Hyponatremia is the most common electrolyte disorder and is associated with brainstem herniation and death. Interestingly, hyponatremia is also associated with cirrhosis  of the liver,  and patients with clinically significant hyponatremia present with non-specific symptoms attributed to cerebral edema, ie. anorexia, nausea and vomiting, lethargy, headache, obtundation,  signs of brainstem herniation , including coma; fixed unilateral, dilated pupils (pupillary responses), decorticate or decerberate  posturing; and respiratory arrest.

A-16 of the record also documents a blood pressure of 121/81 at 0400 hours, while  N-2 of the nurses' notes documents a blood pressure of 112/57 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 responset o 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).

 

HeartPoint Gallery
 

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).

  =blood clotting.

 

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, >60 seconds=Panic) and is elevated in 90% of those with coagulopathy, an increased bleeding tendency due to decreased hepatic synthesis of clotting factor, i.e. with prothrombin ( a protein involved in 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, with an abnormally high alkaline  blood pH  (alkalosis).  Compare Liver encephalopathy.  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. Low numbers of lymphocytes may be seen in different diseases such as hepatitis, lymphoma, or AIDS. 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), also 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. The Mean Corpuscular Volume (MCV) test is usually used to determine what type of anemia a person may have. If elevated, it may indicate anemia from vitamin deficiency such as Vitamin B12 or folic acid. If it is below normal, it usually indicates anemia from iron deficiency.

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 are thus cells that form the primary mechanism in blood clots. Platelets (also known as thrombocytes) coagulate the blood. Platelets plug bleeding capillaries and vessels. With infection, or when the body is cut or otherwise injured, 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. A diminished number of platelets (below the lower limit of normal) is called thrombocytopenia and an elevated number (above the upper limit of normal) is called thrombocytosis. 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. Note that SaO2 alone doesn't reveal how much oxygen is in the blood; for that we also need to know the hemoglobin content.

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” (bloody 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.

criminal negligence...criminal negligence...criminal negligence...

AUTHOR'S NOTES:

The complications of acute liver failure are numerous and include: sepsis, gastro-intestinal bleeding, cerebral oedema, renal and cardiac failure. Pulse oximetry estimates the O2 saturation of the hemoglobin. (Normal is 93 – 97%.) Clinically, increased work of breathing, decreased tidal volume, and increased arteriovenous shunting are manifestations of O2 toxicity. Gastrointestinal bleeding should be controlled if possible and blood purged from the gastrointestinal tract.

The largest amount of O2 content is carried by hemoglobin.
Any reduction in the available amount of oxygen or in hemoglobin will reduce CaO2 and, therefore, oxygen transport to the tissues.Pulse oximetry estimates the O2 saturation of the hemoglobin. (Normal is 93 – 97%.) The largest amount of O2 content is carried by hemoglobin..   Clinically, increased work of breathing, decreased tidal volume, and increased arteriovenous shunting are manifestations of O2 toxicity..
 

Respiratory failure results when the physiological capacity of the respiratory system is less than the body's physiological requirement and can be defined when the arterial PO2 (PaO2) is less than 60 mm Hg or the arterial PCO2 (PaCO2) is greater than 45 to 46 mm Hg. Most clinicians would also define a patient as having respiratory failure if the patient requires supplemental oxygen or mechanical ventilation to maintain blood gases at normal levels. = http://www.mmhc.com/cg/articles/CG0012/sue.html.

A severe headache is a common but not invariable accompaniment of intracranial causes of nausea.. Abdominal pain concurrent with nausea points to the abdomen as the source of nausea..

OXYGEN SATURATION: SaO2..

Binding sites for oxygen are the heme groups, the Fe++-porphyrin portions of the hemoglobin molecule. There are four heme sites, and hence four oxygen binding sites, per hemoglobin molecule. Heme sites occupied by oxygen molecules are said to be "saturated" with oxygen. The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen saturation (in arterial blood, the SaO2). Note that SaO2 alone doesn't reveal how much oxygen is in the blood; for that we also need to know the hemoglobin content..

Other Significant Findings

From the record it is also clear that Arlene Berry endured terrible pain and suffering at the hand of her cruel-hearted egoistic physician, while slowly suffocating to death.

Miss Berry died in part so that Dr. Jordan could test the efficacy of a totally contraindicated neurotoxic brain-damaging psychiatric drug (prochlorperazine), resulting in drug-induced hypoxia with irreversible brain damage due to oxygen starvation of the brain.

Artificial ventilation and oxygen should have been prioritized and promptly administered to include withdrawal of the offending drug, but were not. Instead the patient was seen to be propped up in the arms of two errant nurses (not a recovery position) gasping for air, with only a plastic oral airway in her mouth for quite some time. There was consternation among the nurses - the horrific look on their faces said it all.

When Dr. Jordan finally showed up in the small hours of May 24, 2000, precious moments that followed were not taken up with measures to save his patient’s life, but rather ways to accelerate her demise. He even proposed a DNR (do not resuscitate) order and asked us bluntly if we would prefer to “let nature take its course.” The family was not impressed and so insisted that she be placed on “life” support.

Obviously, Dr. Jordan did not support the use of aggressive interventionist treatment to keep alive someone he had already injured, for to give treatment to remedy a wrong would expose the fact that mistakes were made.

Arlene Berry  was  seen to be the victim of a botched intubation procedure which could have saved her life but instead resulted in internal injury and internal bleeding (e.g. esophageal or lethal gastrointestinal perforation associated with careless instrumention), due to malpositioning of the endotracheal tube which triggered a quick deterioration of her condition; one full hour went by before the error was discovered and the endotrachial tube pulled back.  According to the medical record the intubation procedure was performed by Dr. Jordan, assisted by Helen Studholme, a respiratory therapist.

Following the bungled intubation, Dr. Jordan sought to give the patient coagulation therapy but rather than confine clotting of the blood to the site of the injury,  or perhaps due to his mindless and promiscuous use of inappropriate lab settings, he triggered a “coagulation cascade” of spontaneous sludging of the blood sending numerous “blood-clots” to her brain, resulting in herniation or intracerebral hemorrhage. The levels of fibrinogen, and D-dimer charted in the medical record for May 24, 2000, together with evidence based medicine criterion confirms Disseminated Intravascular Coagulation. 

At a meeting with the coroner in July of 2001 held at the OPP detachement in Kirkland Lake, Ontario, Dr. McLellan admitted to family that there was "no evidence on record of metastatic cancer".  At a subsequent meeting Dr. McLellan provided us with a view of Arlene's prior CT scan that was done in Timmins, Ontario on or about the 16th of March of 2000.  I accompanied Arlene to the Timmins and District Hospital on that date.  A special dye was injected into a vein before the scan was done.  NO clinically detectable metastasis was found.

Further, a mediastinoscopy with biopsy was done on the same date. The result of this testing also proved NEGATIVE.

with respect to the initial CT 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 metastic tumor". According to my research it may also suggest an amyloid deposit which is the hallmark of alzeimers disease, or an old occipital bleed. She would have been asymptomatic. Further submit that the occipital lobes interpret vision. Had it been a tumor there would have been onset visual misperception with visual impairment and subsequent loss of vision with evolution. Arlene Berry had NO visual deficits, indeed she had No focal deficits at the time of her admission to the Kirkland and District Hospital on May 23rd of 2000.

Dr. Mclellan also provided us with a view of a CT which was done at the time of Arlene's death. It shows attenuating collections of blood with massive edema of the right cerebral hemisphere and a 1 cm midline shift that is consistent with Hemorrhagic Stroke, for example. Among causes of hemorrhagic stroke include untreated hypertension, coagulopathies, and ICP (increased intracranial pressure). With the decreased attenuation throughout the cerebral hemispheres due to rapid or spontaneous development of hematomas (blood clots) there would have been little or no perfusion.

Had Arlene Berry been started on corticosteroids to reduce primary brain swelling, and had she been treated responsibly, she would have enjoyed respite from her condition and recovered without further complications. But without timely response due to medical mismanagement and criminal negligence Arlene Berry died unnecessarily.

Further findings suggest that patients with a diagnosis of a primary or metastatic brain tumor associated with a CNS event should have a meticulous review of their history for other possible causes.

The Investigation Continues...