Original article is at  http://victoria.indymedia.org/news/2002/08/7769.php
MANAGEMENT OF IATROGENIC HEPATIC ENCEPHALOPATHY
by Submitted by Malcolm W. Everett • Friday August 16, 2002
 meverett@prweb.com KIRKLAND LAKE, ON
·Iatrogenic hepatic encephalopathy (HE) is defined by the occurrence of brain dysfunction is a direct consequence of a medical intervention (shunt procedures, drugs) in a previously asymptomatic patient with liver disease.

Management of Iatrogenic Hepatic Encephalopathy
PETER FERENCI *
KEY CONCEPTS
· Iatrogenic hepatic encephalopathy (HE) is defined by the occurrence of brain dysfunction is a direct consequence of a medical intervention (shunt procedures, drugs) in a previously asymptomatic patient with liver disease.
· The incidence of HE varies considerably among patients with cirrhosis with or without any shunt procedure.
· In patients treated with TIPS the overall incidence of HE is increased, but the difference disappears when only episodes of overt HE are counted. Spontaneous HE prior to TIPS is the most consistent independent prognostic variable.
· After shunt procedures most episodes of HE are short lived and are amenable to simple medical measures and avoidance of precipitants.
· In few patients chronic HE may be debilitating and requires closure of the shunt. In some, liver transplantation should be considered.
Post-TIPS HE is a problem that may have been overstated. No a routine prophylactic administration of drugs is justified outside of clinical studies.
DEFINITION
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. It should be emphasized that this entity has not been used as a separate diagnosis sofar. To define this condition one has to assume that:
1. a patient with liver disease has normal CNS function before treatment and
2. that HE is a direct consequence of the medical intervention.
In clinical practice, these requirements are rarely met. Normally an apparently asymptomatic patient with cirrhosis experiences a medical problem, receives therapy to improve it, and develops symptoms of HE thereafter. Thus the causal relation between the medical intervention and the appearance of symptoms is circumstantial and cannot be firmly established. Nevertheless, HE occurs frequently following certain treatments such as portocaval shunt procedures or some drugs - these forms of HE can be considered as iatrogenic and will be discussed in this paper. In a broader sense, the term iatrogenic HE could also be used if a medical therapy causes severe liver disease complicated by HE (ie. drug-induced acute liver failure).
The incidence of HE in cirrhotics varies according to the definitions and diagnostic tests applied. By including cases with minimal (subclinical) HE, HE may be present in about 70% of patients ( ). A fairly accurate estimate of the incidence of clinical HE can be derived from controlled studies for treatment of portal hypertension. HE occurred in 0 - 48% of medically treated patients ( ), in 30 to 53% of patients with end to side portocaval shunts, and in 24 - 39% of patients with distal spleno-renal shunts ( , , , ). The variations of the incidence of HE can be best explained by different criteria used to diagnose HE:

* Department of Internal Medicine IV, Gastroenterology and Hepatology
Währinger Gürtel 18-20, A-1090 Wien, Austria
Fax: +43 1 40400 4735, E-mail:  peter.ferenci@akh-wien.ac.at

The diagnosis of overt HE is simple and straightforward. For clinical studies the mental state is graded HE in stages I to IV based on changes in consciousness, intellectual function and behavior ( ). It does not include neurological changes or asterixis. The Glasgow Coma scale is useful in stages III and IV.
In contrast, diagnosis of mild or minimal HE is difficult. Several psychometric tests are used to quantitate mild stages of HE (1, , ). Psychometric testing is more sensitive in the detection of minor deficits of mental function than clinical assessment or EEG (8). However, they are cumbersome and when applied repeatedly the reliability of most of them is adversely affected by the learning effect. Only few are useful in the daily routine. Psychometric tests overdiagnose minimal HE because scores are usually not corrected for age ( , ). The “PSE-index” (2), which combines clinical, psychometric, and laboratory data, has several shortcomings ( ). It does not discriminate between overt, mild or minimal HE and was not validated prospectively. Electrophysiologic tests may be useful to quantify overt HE in studies. In conventional EEG tracings the degree of abnormality can be graded semiquantitatively. Computer assisted techniques can quantitate variables such as the mean dominant EEG frequency or the power of a particular EEG rhythm. Evoked or event related responses, like the P300 peak after auditory stimuli are sensitive to detect subtle changes of brain function and can be used for diagnosis of minimal HE ( ).
INCIDENCE OF IATROGENIC HEPATIC ENCEPHALOPATHY:
The incidence of minimal HE varies considerably among patients with cirrhosis (see table 1). Most frequently, procedures that create a wide shunt between the portal- and systemic venous circulation to decrease portal pressure may increase the incidence of HE. But also some drugs may affect brain function in a manner undistinguishable from HE.
Shunt-Surgery and TIPS
Although it is conventional knowledge that any shunt procedure may increase the risk to develop HE, the published data not always support this assumption. Several factors may explain such discrepant findings and include patient selection (assessment of pretreatment brain dysfunction), criteria and tests for diagnosis of HE, the length and frequency of the follow up, as well as the treatment of control and study groups. The results on the frequency of HE in various prospective, randomized trials are listed in table 2. Some of the data were quite surprising. For example the incidence of HE in patients treated with endoscopic sclerotherapy was 3 fold higher in studies using TIPS than in those with distal splenorenal shunt. The rate of HE was not different when distal splenorenal shunt was directly compared with end-to-side portacaval shunt, although all textbooks state that distal splenorenal shunt has a much lower incidence of HE.
In patients treated with TIPS the overall incidence of HE is increased, but this difference disappears when only episodes of overt HE are counted. Spontaneous HE prior to TIPS is the most consistent independent prognostic variable predicting its development and should therefore be a relative contraindication for TIPS
Drugs
Although drug-induced HE is always discussed, actual data are quite scarce. The best evidence for drug-induced HE is documented for benzodiazepines. The role of benzodiazepines for the pathogenesis of HE is still under discussion (for review: 12). Rats with liver failure are more sensitive to the sedative effects of benzodiazepines than normal rats ( ). Similarly, in humans an increased sensitivity of patients with cirrhosis to benzodiazepines was clearly documented ( ). After an ordinary sedative dose (0.25 mg) the apparent oral clearance of unbound triazolam was lower in cirrhotics than in controls.

Clearances correlated with severity of liver disease. At a time when plasma concentrations of unbound triazolam were the same as in controls (2.25 hr after dosing), flicker sensitivity at 5 Hz and the digit symbol substitution test were impaired in cirrhotics. In patients dying with HE t exogenous administered benzodiazepines was accounted for the presence of benzodiazepines in brain tissue ( ).
Other drugs which may precipitate or worsen HE are loop diuretics ( , ), propranolol ( , ) and ketanserin ( ).
TREATMENT OF IATROGENIC HEPATIC ENCEPHALOPATHY
Drug-Induced Hepatic Encephalopathy
The treatment of choice in benzodiazepine-induced HE is the use of flumazenil (12). If tranquilizers are needed in patients with cirrhosis potential side effects can be reduced by using lower doses. For other drugs usually a supportive therapy is sufficient to allow the excretion and /or metabolic inactivation of the drug to take place.
HE AFTER PC-SHUNT PROCEDURES
Overt Hepatic Encephalopathy
After shunt procedure, most episodes of HE are short lived, do not require admission to hospital, and are amenable to simple medical measures such as lactulose and avoidance of precipitants ( , ). New onset HE is clustered around the first month after TIPS insertion and improvement of neurological status was observed in a significant number of patients during follow up.
Chronic spontaneous encephalopathy develops in about 10%. In addition of standard measures, protein restriction in combination with supplementation of the diet with branched chain amino acids may ameliorate the condition of the patients. Beyond that, drug treatment may be helpful in selected cases. Bromocriptin or oral flumazenil were effective in single cases ( ) and cannot be generally recommended. If the condition is sufficiently debilitating it requires closure of the shunt. This can be done using reducing stents, LGV filters or coils, but when these measures fail, suggesting that deteriorating liver function is the cause of the encephalopathy, liver transplantation should be considered.
Minimal Hepatic Encephalopathy
Although the number of patients with minimal HE is large, good clinical studies are rare. Even among experts, there is no agreement how to define minimal HE or whether minimal HE exists at all. Efficacy of treatment is judged by the improvement of psychometric tests or of electrophysiologic measurements. The impact of these parameters and the benefit of their improvement for the patients is uncertain. Substances that modify psychometric tests in prospective studies include lactulose ( , ), ornithin-aspartate ( ) and oral BCAA ( , ). A need for treatment of minimal HE is not established and should only be used in controlled clinical trials. There is no single study addressing reasonable treatment endpoints such as improvement in quality of life. Good clinical studies are badly needed.
Prevention of HE in patients with PC-shunt procedures
Post-TIPS HE is a problem that may have been overstated so far. Not a single study has been published sofar to justify a routine prophylactic administration of drugs to decrease the likelihood of the occurrence of HE after the procedure. Certainly the best prophylaxis of HE is to select patients carefully for TIPS placement. In patients with a high-risk profile (Child class C, pretreatment HE, age >65 years) all other treatment options should be explored and TIPS should only used as last resort.

Table 1: Frequency of abnormal test results (in %) in patients with cirrhosis without overt signs of hepatic encephalopathy (only studies using age adjusted normal values listed).
Autor (Ref) N NCT Symboldigit other spectral EEG evoked responses
Weissenborn (10) 130 17
Quero (11) 137 7 5 17
Groeneweg ( ) 179 9 3 19
Yang ( ) 61 31 47.5
Amodio ( ) 100 19 Posner-test: 17 40
Amodio ( ) 94 21 Choice 2: 20Scan: 23
NCT: Number connection test A

Table 2: Frequency of HE in patients with cirrhosis and shunt procedures (only in prospective controlled trials)
Surgery Endoscopy TIPS Medical treatment OR
DSRS vs. ET ( ) Chronic HE:16Acute HE: 7 Chronic HE:9Acute HE: 6 1.9 (1.1-3.6)NS
PC-Shunt vs. Control ( ) Prophylactic: 45Therapeutic: 35 Prophylactic: 28Therapeutic: 7 2.0 (1.2-3.1)4.9 (2.1-11.3)
PC-Shunt vs. DSRS 1.3 (0.8-2.2)
ET vs.TIPS ( ) 19 34 0.43 (0.3-0.6)
DSRS= distal splenorenal shunt; ET: endoscopic therapy; OR= Odd´s ratio (95% confidence interval)
A CASE IN POINT
THE ARLENE BERRY DEATH COVERUP
by Malcolm W. Everett • Friday, August 16 2002
 meverett@prweb.com KIRKLAND LAKE, ON

THE ARLENE BERRY DEATH COVERUP
M. W. Everett
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.
Introduction:
Publication in good faith for redress of wrong
315. No person shall be deemed to publish a defamatory libel by reason only that he publishes defamatory matter in good faith for the purpose of seeking remedy or redress for a private or public wrong or grievance from a person who has, or who on reasonable grounds he believes has, the right or is under an obligation to remedy or redress the wrong or grievance, if
(a) he believes that the defamatory matter is true;
(b) the defamatory matter is relevant to the remedy or redress that is sought; and
(c) the defamatory matter does not in any respect exceed what is reasonably sufficient in the circumstances.

Updated Aug15, 2002
INVESTIGATIVE REPORT
The Arlene Berry Case
RE: Arlene H Berry
Date of Death: May 24, 2000
Forward
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
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 Compare the medical record of Arlene Berry for May 23rd and May 24th of 2000.
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-54 documents a recent history of hematuria (blood in urine) for three days and a prescription for CIPRO, an antibiotic used for treatment of UTI (urinary tract infection), also indicated in the treatment of a variety of infections including influenza. The same record documents “blood when voiding”, that she was on antibiotics for 1 week and that she was given CIPRO, “1 given now”. The same record also documents nurses’ observations of “large blood trace leukocytes”.
The same physician (whose signature is illegible) made a notation with respect to the flu, which was directed to the attention of the patient’s family MD (Dr. Jordan). From this record, it is clear that the physician who saw her made made a diagnosis of UTI. The test result from that diagnosis 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.
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 evidenced at A-21 of the medical record.
What I take to be a continuation of the same record at A-23 documents that her speech was observed to be “slurred”, also a sign of toxicity. The record at OP-54 dated May 22nd of 2000 documents a “haggard” appearance including “large blood trace leukocytes”. White blood cells (leukocytes) are elevated with dehydration, 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.
The outpatient record at OP-53 documents that she was pale-looking and lethargic and
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-5 documents 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-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 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–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. At the time of her admission to the hospital her BP (blood pressure) at A-6 of 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-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 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 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. 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–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. The same record also documents a rapid drop in blood pressure to 98/70 at 0235 hours with physician “assessments unchanged” despite the fact that the patient had already gone into respiratory distress as evidenced by “Cheyne-Stokes” respirations with periods of apnea lasting 5-8 seconds. Notably, the central mechanisms that regulate breathing fail in severe hypoxia leading to irregular respirations, Cheyne-Stokes breathing, apnea, and respiratory cardiac failure (hypoxia leads to obtundation). Notably, there is nothing on record to suggest that the patient was oxygenated prior to intubation and from these records it is clear that the health care providers withheld life support when the patient became critically ill.
The same record at 0255 hours documents a “sudden large bloody emesis of reddish brown” what is known in medical circles as “coffee-ground vomitus” (dark brown vomitus the colour and consistency of coffee-grounds composed of gastric juices and old blood) indicative of a slow bleeding source in the upper GI tract. Notably multiple medications, restricted diet or poor nutrition causes gastrical intestinal (GI) lesions to GI bleeding. Further, GI bleeding is considered a potential medical emergency. From that record, it is clear that nothing was immediately done to determine a possible cause or treat accordingly and that Dr. Jordan showed no concern for this patient is spite of her worsened condition. Also, Dr. Spiller (the ED physician) did nothing to lessen or prevent the outcome, suggestive of his complicity or acquiescence to test the efficacy of the given drug (Stemetil) or outright incompetence or other negligence.
The record at N–4 documents the patient’s “transfer to ICU” at 0320 hours. The record at A-27 documents a blood pressure of 163/117 at the very same time. The presence of severe elevation of blood pressure with a diastolic blood pressure greater than 120mm Hg is considered a hypertensive urgency that requires reduction.
The record at A-24 documents the charting of the patient’s vital signs that commenced recording at 0315 hours. It is interesting to note that the patient’s transfer to the ICU had not yet taken place, that no attempt was made by the healthcare providers to place the patient in the ICU prior to 0320 hours and further that the patient’s condition remained critical throughout the night and into the small hours of the morning notwithstanding. The same record documents a heart rate (HR) of 174 bpm at 0320 hours that is consistent with trauma.
From these records alone it seems clear that the healthcare provider had done too little too late as evidenced by the records at N–9, N–10, N–11 including A-3 and A-21.
The record at N-4 documents “incontinent blood tinged urine” at 0305 hours that is consistent with hematuria and ‘large blood trace leukocytes” documented at OP-54, while N–3 of the record documents a ‘large amount of dilute urine’ at 0325 hours, only 20 minutes later and again at 0450 hours as documented at N-1 that is inconsistent with the record as a whole and in particular with respect to A-16 marked by a complete absence of documentation as to water refill as to justify urine output, evidenced by the complete absence of documentation for “elimination” seen at N–10 of the record.
There are numerous material deficiencies in the related medical records in which several pages of documentation manifest a lack of internal consistency ranging from out of sequence reports such as the triage record seen at A-5, to obviously rewritten, altered and falsified nursing notes seen at N–1, N–2 and N–3, marked by error, inconsistency and contradiction, to the ventilation record seen at A-16 and A-17 presenting similarly. The physicians diagnostic sheet at A-3 ought to have been placed on the record at the time of the patient’s admission as well as the emergency record seen at A-4. Notably, both of these records were dated using a rubber stamp. Further, the ambulance call report was filed on the record at N–7 and N–8 of the nursing notes. That document ought to have been placed on the patient’s file on or about the time of the patient’s discharge.
The record at A-6 documents the patient as having a history of metastatic lung cancer, while the record at OP-54 documents “NO MESTASIS”, and medianastoscopy “NEGATIVE”.
There are several late dictations, all of them questionable and I can count at least 3 in all seen at A-1 and A-2, 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 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). Ref:  http://www.emedicine.com/EMERG/topic176.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-16 documents a BP of 163/117 at 0330 hours, while N–3 documents a BP of 136/85 at the very same time.
At 0352 hours the patient’s blood pressure was documented at 85/52, some 17 minutes later, as evidenced at N–2 (in which blood pressure is inadequate for normal perfusion and oxygenation, to rule out prompt replacement of blood and fluid volumes). According to my investigation, at the point of loss of blood pressure the resulting end organ injury is often irreversible i.e., endothelium, lung, kidney, liver, etc.
A-24 of the record documents a heart rate (HR) of 154 at 0330 hours, while the Ventilation Record at A-16 documents at HR of 126 at the very same time, a significant difference.
From these records it is clear that nothing was done to bring the patient’s BP under control in a timely manner and would have resulted in permanent brain damage at that point. According to my research, there would have been a loss of perfusion and autoregulation with the rapid drop in BP and it is also clear that nothing was immediately done to correct it. It is interesting to note that adequate cerebral perfusion must be restored within 3-5 minutes for complete neurological recovery.
The physician’s critical care note, a late dictation which purports to have been dictated at 0420 hours on May 24th of 2000 seen at A-8 of the record documents “later that evening she rapidly deteriorated and became unconscious without responding to verbal stimuli or painful stimuli”, while the record at N–2 of the nursing notes documents “attempts to pull away to painful stimuli” at 0400 hours only 20 minutes earlier.
(Note: I had asked the patient in the presence of her foster brother, if she could hear me to wiggle her toes and she did, not once but twice. In my opinion, she appeared to be more paralyzed than anything).
A-16 of the record was initialled by both Helene Studholme and Janice Chamaillard. The latter is the author of N–1 through N–3 of the record, and the co-author of A-16 while 75% of the ventilation record was authored by helene Studholme. The two versions of the patient’s vital signs is proof of deception, and fabrication on the part of healthcare providers.
What I take to be the physician’s lab record at A-24 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.
What I take to be the Cardiac Index at A-18 documents the patient’s vent rate at129 bpm at 0417 hours with heart and breath rate increased (sinus tachycardia) that is consistent with systemic inflammatory response to clinical insult such as caused or worsened by medications suggestive of 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).
What I take to be a summary of the physician’s lab work 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 (> Court of appeal >>
R. V. MANJANATHA, (1995-06-21) SKCA CA95081