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 manufacturer'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-16documents 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 response. 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 as being "55" years when in fact she was only 41 years of age.

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

The aPTT (coagulation partial thromboplastin time) a test used to determine the efficacy of various clotting factors used in the diagnosis of blood coagulation disorders documents the therapeutic range for Heparin therapy at 60-100 seconds (23-35 is the normal, >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 dehydrationhyperviscosity 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?7%.) 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.