Wednesday, May 13, 2009

Creatine Kinase: Factbites

Creatine Kinase Factbites

Creatine Kinase
(CK) is the most sensitive enzyme and in the presence of most diseases, levels can be elevated as much as 50 to 100 times the reference level.

CK is often determined routinely in emergency patients. In addition, it is determined specifically in patients with chest pain and acute renal failure. Normal values are usually between 25 and 200 U/L. This test is not specific for the type of CK that is elevated. In females, total Creatine Kinase should be 10-79 units per liter (U/L).

Elevation of CK is an indication of damage to muscle. It is therefore indicative of injury, rhabdomyolysis, myocardial infarction, myositis, myocarditis, malignant hyperthermia and neuroleptic malignant syndrome.

Creatine kinase (CK or CPK) is an enzyme or type of protein found in muscle and brain that leaks out and is released into the bloodstream when muscle is damaged. CK helps cells make the energy needed to move: may also be tested from the patient's medical record. The CK level usually parallels a disease activity.

In normal conditions, there is very little creatine kinase circulating in the blood of the average, healthy human being.

Muscle wasting is a hallmark of a number of diseases, including cancer, bacterial sepsis, AIDS, diabetes, and end-stage heart, kidney, and obstructive pulmonary disease. Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients. Skeletal muscle atrophy is a common comorbidity of cancer. The progressive depletion of skeletal muscle is a hallmark of many types of advanced cancer. However, a clinical feature of demyelination is muscle weakness without muscle atrophy.

Guillain-Barré syndrome and similar disorders do not produce evidence of muscle inflammation, such as elevation of the CK. Hypokalaemic periodic paralysis has a predilection for thyrotoxicity in some patients. It is associated with a low potassium concentration but it too is associated with a normal creatine kinase level.

Persons with cancer typically have high CK levels.

Metastatic malignant neoplasms cause severe body wasting-cachexia. The hallmark of muscle damage or muscle wasting is elevation of CK concentration. The wasting away of fat and muscle (cachexia) is the most visible hallmark of metastatic cancer.

Elevation of CK may be seen in stroke, extreme shock, or brain tumor(s). A very high creatine kinase value indicates severe muscle fiber breakdown (necrosis). Even in paraneoplastic disorders the serum CK level is typically elevated 8-100 times normal. Persistent or ongoing muscle injury will maintain high CK concentrations.

The hallmark of muscle damage is elevation of creatine kinase ( CK ) concentration, which is also present in all patients with rhabdomyolysis. During episodes of acute muscle breakdown (rhabdomyolysis), CK levels can temporarily go off the scale, topping out at 50,000 to 200,000 U/L.

Other forms of muscle damage, such as from a fall, a car accident, surgery, or a shot, can also increase CK. CK levels usually rise significantly in about 2 to 3 hours or perhaps a little longer (can rise two-fold within six hours) and peak within 24 hours. High CPK levels may be seen in patients who have: Heart attack; Brain injury or stroke.

See also

Creatine kinase test | Encyclopedia of Medicine | Find Articles

Elevated Serum Creatine Kinase

Creatine kinase BB: a new tumor-associated marker

Creatine kinase testing

Abstracts: The diagnostic and prognostic value of pretreatment

Cancer of the Nervous System

Saturday, May 2, 2009

Creatine kinase (CK)

Creatine kinase (CK or CPK) is an enzyme or type of protein found in muscle and brain that leaks out and is released into the bloodstream when muscle is damaged. In normal conditions, there is very little creatine kinase circulating in the blood of the average, healthy human being.

CK is the most sensitive enzyme and in the presence of most diseases, levels can be elevated as much as 50 to 100 times the reference level.

Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients. Even in paraneoplastic disorders the serum CK level typically is elevated 8-100 times normal.

Skeletal muscle atrophy is a common comorbidity of cancer. Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients and the progressive depletion of skeletal muscle is a hallmark of many types of advanced cancer.

Guillain-Barré syndromeis a disorder caused by "nerve" inflammation (not muscle inflamation), involving progressive muscle weakness or paralysis. GBS initially does not usually produce evidence of muscle inflammation or waisting such as elevation of Creatine Kinase (CK) concentration. Persons with GBS or clinically similar disorders typically have normal or low CK levels at onset of the disease, unless tissue damage in the brain or elsewhere has already occurred.

To illustrate, a low/normal CK at the time of a patient's admission to hospital would argue favourably against a diagnosis of structural brain damage, or active metastatic cancer.

A clinical feature of demyelination is muscle weakness without muscle atrophy. Persons with Muscular Dystrophy, Guillain-Barré Syndrome and other neuromuscular disorders typically have low creatine kinase levels.

Lyme disease may also cause weakness secondary to peripheral neuropathy but it too does not produce evidence of muscle inflammation such as elevation of the CK.

Creatine Kinase (CK) should typically not be elevated in GBS and if it is, another cause (or underlying disorder) should be suspected.

The highest creatine kinase activities are found in skeletal muscle, myocardium and brain tissue. Significantly increased creatine kinase levels may support a hypothesis of brain death; normal CK levels do NOT.

In females, total Creatine Kinase should be 10-79 units per liter (U/L). CK is the most sensitive enzyme and in the presence of most diseases, levels can be elevated as much as 50 to 100 times the reference level.

narcotic analgesics and laxitives

Coadministration of narcotic analgesics with laxitives may have additive central nervous system (CNS) and gastrointestinal (GI) system effects, and increase the risk of severe constipation or paralytic ileus, including CNS depression.

Migraine headaches

Migraine headaches happen when blood vessels in your head open too wide or close too tight. The most common triggering agents for migraines are alterations in serotonin metabolism (deficiency), diabetic condition, hormonal imbalances, histamine-induced platelet aggregation (blood platelets sticking together), blood sugar imbalances and certain medications.

In women, migraine attacks may also be triggered by hormonal changes during menstruation (periods).

Ameboma, the forgotten granuloma?

Consider a cyst that occupies space and feeds off red blood cells ... giving rise to purulent matter resulting in dessemination and abscess formation. You are encouraged to think critically about what you find here. Do your own research if you still have questions.

Amebiasis is a disease caused by a one-celled parasite called Entamoeba histolytica (ent-a-ME-ba his-to-LI-ti-ka). There are a number of variants.

In the Canada and the United States, amebiasis is most often found in immigrants from developing countries. It also is found in people who have traveled to (or who have come into contact with) developing countries, such as Mexico.

The symptoms often are quite mild and can include loose stools, stomach pain, and stomach cramping. Amebic infection is a severe form of amebiasis associated with stomach pain, bloody stools, and fever. Rarely, E. histolytica invades the liver and forms an abscess. Even less commonly, it spreads to other parts of the body, such as the lungs or brain, and cause abscesses. It may produce symptoms that mimic a number of intestinal disease processes, including cancer.

The infection may mimic space-occupying lesions in CNS, and the infected patient may present with hemiparesis, aphasia or seizures. In such instances, head CT and MRI may reveal ring-enhancing lesion (abscesses) suggestive of brain tumors. Parasitic cysts of any origin may mimic primary or metastatic brain tumor(s).

Clinical Features:
A wide spectrum, from asymptomatic infection ("luminal amebiasis"), to invasive intestinal amebiasis (dysentery, colitis, appendicitis, toxic megacolon, amebomas), to invasive extraintestinal amebiasis (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions). An ameboma may mimic carcinoma of the colon.

Pleuropulmonary amebiasis is the common and pericardial amebiasis the rare form of thoracic amebiasis. Pleuropulmonary amebiasis is easily confused with other illnesses and is treated as pulmonary TB, bacterial lung abscesses, and carcinoma of the lung, which may exacerbate the condition.

Amebiasis is caused by the protozoan parasite. Protozoan infections include amebiasis, toxoplasmosis, and trypanosomiasis (sleeping sickness). Protozoa can produce malaria, amebiasis, leishmaniasis and trypanosomiasis.

Typically, N fowleri produces primary amebic meningoencephalitis (PAM), which is clinically indistinguishable from acute bacterial meningitis.

The cyst fills with bacteria and pus, and becomes an abscess (chocolate-brown abscess fluid is thought to be highly characteristic of amebic abscess); the earliest amoebic lesions appear as small, yellow mucoid (yellowish exudate) elevations containing necrotic material where the parasite can be found. The center of an amebic abscess, consisting of lysed hepatocytes, erythrocytes, bile and fat, may liquify and this necrotic material (sometimes incorrectely called pus) will range in color from yellowish to reddish brown. If the abscess bursts inside the body, there is a risk of blood poisoning (septicaemia). Septicemia, is a form of sepsis.

The most common signs of amebic infection are alternating diarrhea and constipation(possibly accompanied by blood and excessive mucus) and irregular appetite. Other clinical signs include vomiting, listlessness,weakness, low weightand signs of dehydration (e.g.sunken eyes, thick oral mucus). If the lungs are infected (a condition generally associated with more chronic infections), labored breathing, mouth/nasal discharge and wheezing may also be noted.

In the Canada and the United States, amebiasis is most often found in immigrants from developing countries, such as Mexico. It also is found in people who have traveled to (or who have come into contact with) developing countries and in people who live in institutions that have poor sanitary conditions which pose health issues for travelers.

Ameba only multiplies rapidly if a person is very run down by an immune deficiency, illness or infection. Only virulent amoeba can lyse polymorphonuclear leukocytes (PMNs).

Ameba can spread hematogeneously from a cutaneous, ocular, or pulmonary lesion to the CNS, where vasculitis may also dominate the clinical picture.

An ameboma may simulate an "adenocarcinoma" or another granulomatous process. Parasitic cysts of any origin may mimic primary or metastatic brain tumor(s).

immigrant doctors

Many immigrant doctors who come to Canada have very low qualifications. Many of them have been exposed to malaria, parasites and unfamiliar infectious diseases, such as amebiasis and also pose public health risks from a variety of emerging infectious diseases.

Mexico is a hotbed for amebic infection (amebiasis ), a source of infectious cysts.
Some doctors may be carriers and not even know it.

WARNING: Parasitic cysts of any origin may mimic primary or metastatic brain tumor(s).

Friday, May 1, 2009

Altered & Falsified Medical Records


Fraudulent addition
to a medical record for the purposes of covering up an incident can be detected by current technology. Expert document examiners will need the original medical record in order to analyze it for tampering. This will enable them to detect differences in ink, look for indentations caused by writing on sheets above the questioned document, and perform chemical analysis of the document. There are clues used
to detect altered records.

Clues to altered records:
  • writing crowded around existing entries

  • changes in slant, pressure

  • uniformity or other differences in handwriting

  • erasure or obliteration

  • use of different pens or typewriters to write one entry

  • misaligned typed notation, impressions or lack of impressions from writing instruments on the following pages

  • ink offsets or lack of offsets on the back side of the preceding page, and

  • additions on different dates written in the same ink, while original entries were written in different ink.

All health care professionals should be aware that falsification of medical records is grounds for criminal indictment.

Case In Point:

The evidence speaks when victims cannot

Altered Medical Records

In Memory of Arlene Berry 1958-2000

“Truth cannot live on a diet of secrets withering within entangled lies” H. Michael Sweeney

The Quest for Medical Truth

Part I

The Arlene Berry Death Coverup

These are the facts:

There are numerous material deficiencies in the related medical record of Arlene Berry which manifest a complete lack of internal consistency ranging from out of sequence records, from the physician s Critical Care note to the nurses Triage to obviously rewritten, altered and falsified medical records seen between N-1 and N-3 of the nurses notes, including the physician’s Lab Report, marked by error, inconsistency, omission, and contradiction that is consistent with telling lies, to the Ventilation Record seen at A-16 and A-17, presenting similarly.

The record at A-6, what I consider to be quite contradictory, documents a “history of metastatic lung cancer” while the record at OP-54 clearly documents “no metastasis” and “mediastinoscopy negative”.

The Ventillation record contains a self-serving entry, ie. “without adversities” relating to patient’s intubation procedure, which took place at 0325 hours on May 24th of 2000, while the record at A-17 documents patient being “suctioned for moderate amounts of coffee ground emesis” at 0330 hours, only five minutes later, which can suggest thoracic injury, or perhaps a severe gastrointestinal problem, or both. That the patient’s Heart Rate soared to 174 bpm during the intubation procedure should be borne in mind. I find this to be very significant in terms of iatrogenic injury.

An example of going a step further, requires a high index for suspicion of iatrogenic injury which may become more readily apparent after following a time course for events, “before and after” , which in this case is marked by hypotension preceded by evidence of hypertension and is evidenced by a documented blood pressure of 162/80 at 0220 hours followed by a lethal drop in blood pressure to 78/70 by 0235 hours that is a hallmark feature of orthostatic hypotension in which BP rises or falls significantly. Another example is a documented BP of 163/117 at 0320 hours that by 0352 hours dropped to 85/52, with much of the record presenting similarly.

N-4 and N-5 present with less than half a page of documentation that is consistent with deliberate omission, such as withholding information.

A-24 and A-25 of the record, what I take to be identical forms, appear to be misaligned when superimposed (one over the other) and held over a light. Further, the print sizes appear to be slightly different and both are marked “Page 1 of 1”, to rule out conformity and consistency. Further, A-14 shows a misaligned margin suggesting a split in the page, or perhaps a cut out, with A-13 and A-27 presenting similarly.

Many of the records contain write-overs, primarily with respect to date and time, suggesting that perhaps the authors were no longer oriented to date and time of events that is consistent with making changes at a later date.

According to the Certificate of Death Arlene Berry died on May 24th of 2000. According to her physician “she died several days later with numerous metastatic lesions to her brain”. However, the medical record for May 23rd and 24th of 2000 tells a very different story, suggestive of a known “resistant bacterium” of the Staph aureus variety with a sepsis-like picture that is consistent with a severe hospital acquired infection or a bacterial meningitis. Further examination of the record reveals evidence of “iatrogenic neglect” (doctor caused negligence) and outright incompetence on the part of the healthcare providers to say the least, that is consistent with substandard care.

There is a complete absence of record with respect to the patient’s blood pressure between 1845 hours on May 23rd and 0040 hours on May 24th of 2000. This can suggest either incompetence or deliberate omission and can also constitute evidence of substandard care. lA-26 of the record documents a BP (blood pressure) of 78/70 at 0235 hours, while N-5 documents a BP of 98/70 at the very same time suggestive of having been copied.

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. The same record documents a BP of 121/81 at 0400 hours, while N-2 documents a BP of 112/57 at the very same time that is also consistent with copious error.

A-24 documents a Heart Rate (HR) of 154 bpm at 0330, while the Ventilation Record documents a HR of 126 bpm at the very same time, a significant difference. The same record documents the mechanical charting of the patients vital signs commencing at 0315 hours on May 24th of 2000. It is interesting to note that the patient’s transfer to the ICU had not taken place until ten minutes later at 0325 hours. I would really like to know how they were able to proceed with the recording of the patient’s vital signs in her absence.

A-4 of the record, what I take to be a Trauma Legend, barely visible in the physician’s notes situated at the lower right hand side of that record there is an obliterated area suggesting a white-out or perhaps an erasure. This to me suggests that was was indeed trauma involved.

A-1 of the record documents “she had a left lung pneumonectomy back in October of 1999”, which is erroneous. A-17 documents the very same error with “removal of left lung in 99”, suggestive of having been copied. The bald truth is that the patient was last seen by the same physician who originally had misdiagnosed her in October of 1999 for which she had the lung removed on January 13th of 2000.

A-3 of the record, what I take to be the physician’s diagnostic chart is a total blank. From that record it seems clear that nothing was entered because nothing was done. The same record was filed out-of-sequence. The emergency record at A-4 was also filed out-of-sequence. Interestingly both of these records were dated using a rubber stamp that is consistent with backdating.

A-1 of the record documents “I was called in later that night because the patient had become obtunded”, while N-6 documents “no response to deep pain” as early as 0030 hours on May 23rd of 2000. N-4 of the record documents that Dr. Jordan was notified of patient condition at 0225 hours, while N-2 documents “attempts to pull away to painful stimuli” at 0400 hours on May 24th, one hour and thirty-five minutes later, after the time the physician claims he was called in. There can be no question that the doctor lied.

There is a complete absence of documentation with respect to the patients bowel routine and urinary elimination pattern for toileting as evidenced at N-10 of the record, with the very same information omitted at OP-53 of the record.

Caveat: There are two precautions on record for what I take to be a warning with respect to “resistant bacteria”. The precaution can be seen more visibly at N-9 of the record under the subheading for “INFECTION CONTROL PRECAUTIONS”, evidenced by a check mark in the box. Notably, the particulars with respect to type of resistant bacterium are omitted. A “resistant bacteria” denotes a very serious infection of the “super-bug” antibiotic resistant variety, usually hospital acquired.

In a letter to the College of Physicians and Surgeons of Ontario dated November 28, 2000, Dr. Jordan writes “discussed the situation with family members and a decision was made to intubate Ms. Berry”, while the Ambulance Call Report documents an unsigned physician order to withdraw life support from an obviously critically ill patient, as evidenced by an obscure and secretive 3.3 Code only to be found in the annals of internal medicine. In acting as aforesaid it seems clear that Dr. Jordan ordered her death.

The record at N-6 documents bilious vomit at 1915 hours following the patient’s admission, as evidenced by “emesis of >> 100 cc yellowish fluid” that is the hallmark of intestinal obstruction that by 0330 documents “moderate amounts of coffee ground emesis” that is consistent with upper gastrointestinal bleeding. Another record documents a “large bloody emesis of reddish brown”, and “orally thick secretions” suggestive of a more significant backup of intestinal material, while the Ambulance Call sheet at A-7 documents an “intracranial bleed” that is inconsistent with the hospital record as a whole. This infers a blatant attempt tp obfuscate the truth.

The record at A-8 and A-9 documents “Medi-Vac team were due to arrive at 0435”, while the Ambulance Call sheet documents the time of the call event for ”call received at 0620” hours, a significant difference.

There are several late dictations and I can count at least three two page documents, all of them questionable seen at A-1, A-2, A-6, A-7, A-8, and A-9, as evidenced by the times and dates upon which they were dictated and transcribed. One of them was dictated in June of 2000, and transcribed in July of 2000, some two months after the patient s death. lThe Cardiac Index falsely documents the patient’s age at “55 years”, she was only 41.

N-7 documents a “stable” condition. Yet the same record documents a complete withdrawal of life support from a critically ill patient as evidenced by a Code 3.3, including a Nature Code 0 that is consistent with No Care.

The Ambulance Call report also documents a “pale, dry and cool” condition that is consistent with clinical manifestations of adrenal insufficiency, or hypovolemic shock. Compare Shock Syndromes in which pallor and cold peripheries suggestive of vaso-constriction all point to circulatory failure.

The same record at N-7 documents pulses X 4 good; head and neck OK; chest OK; abdomen OK; pelvis OK; extremities OK. The “coffee ground emesis” (suggestive of old blood and gastric juices) including the “large bloody emesis of reddish brown” and “ orally thick secretions” (suggestive of a more significant backup from the intestinal tract) associated with abdominal bleeding documented elsewhere on the record were completely omitted from the ambulance call record and substituted for “intracranial bleed”.

According to Dr. Jordan “she was admitted by Dr. Spiller with symptoms suggestive of metastatic CA of the brain”. According to Dr. Spiller ”a question has been raised” with respect to metastatic cancer of the brain. According to the record she was admitted for “vomiting”. Vomiting is not a diagnosis, but rather a symptom of many causes. The buck-passer, let us agree, tries to pass the buck together with all the possible blame for not having the right answer.

Much of the record is illegible. Illegible writing is reckless writing suggestive of callousness, ie no quality in writing, no quality in care. It also explains why many medical records are rewritten, after the fact, but which also affords opportunity for malfeasance to those who would dare skew the record in order to save face.

No autopsy was done. A family request for a formal inquest into the denied. cause of the patient’s death was also denied

Worthy of mention is that there is absolutely nothing in the patient’s blood values to even remotely suggest metastatic cancer, although a leukomoid reaction is a distinct possibility. In fact , everything points to a severe undiagnosed and untreated hospital acquired infection with a sepsis-like picture suggestive of the Toxic Shock Syndrome or staphilococcal meningitis, including evidence of neuroleptic drug involvement.

From the record it seems clear that the healthcare providers failed miserably in their concerted efforts to obfuscate the truth. Not only did they act together, but together with malice and forethought and with intent to defraud the estate of the deceased of any lawful claim they may have had against them (the doctors and nurses) for their part in substandard care and civil wrongdoing. They unwittingly escalated their plot into a criminal conspiracy and criminal wrongdoing of all kinds by their own doings. Perhaps its time they all had their moral codes thoroughly overhauled.

Altered Medical Records
by meverett Wednesday, Aug. 03, 2005 at 6:38 AM

The following Supporting Information is available for this article:

LSU Law Center's
Medical and Public Health Law Site
Articles on Law, Science, and Engineering
Scientific Misconduct: Part 3 - Standards for Scientific Record Keeping

add your comments

falsified medical reports
by Amy Lynne Friday, Sep. 30, 2005 at 9:49 AM

I found this site while trying to research the prevalence of falsified medical documents...

I have experienced the death of a loved one, my 2 year old son, and have discovered false and contradictory statements from the ambulance report, which logically explains the confusion and mis-diagnosis at the hospital where they did not treat my son based on his actual condition or a truthful account of events leading up to his arrival at the hospital.

I do not know how to go about reporting this injustice, as there seems to be nobody who is willing to investigate this. Although the sequence of events in the report is impossible and illogical, and directly related to our son's needless death, our lawyer advises against persuing a lawsuit because the possibility of a small and limited court award does not justify the vast expense involved in the legal process and the possible risk of financial loss in the event that the case is lost.

More people should insist on laying criminal fraud charges in such cases. The main purpose of altering and falsifying medical records is obvious - to "dupe" the injured party or in the case of death his/her estate or next of kin of any lawful claim they may have had. My advice is to go for it.

Detecting Tampering with Medical Records

Articles From IEEE Engineering in Medicine and Biology Magazine
Scientific Misconduct

View the medical record of Arlene Berry

physicians' attitudes: deception

Physicians' attitudes toward using deception to resolve difficult ethical problems

To assess physicians' attitudes toward the use of deception in medicine, JAMA sent a questionnaire to 407 practicing physicians. "One third indicated they would offer incomplete or misleading information to a patient's family if a mistake led to a patient's death." JAMA Vol. 261 No. 20, May 26, 1989

Mean Cost Per Patient With Guillain-Barré syndrome

The mean cost per patient with Guillain-Barré syndrome has been estimated at $318,966 US. The cost to treat a patient with Fulminant GBS may be significantly higher.

Send your tips, stories and ideas: