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Spinal Cord Nerve Damage Caused by Lead and Arsenic Poisoning Misdiagnosed as Multiple Sclerosis.
I will discuss the medical care prospectively, and have selected the key pages and underlined the most significant facts, which will assist your understanding of this case. Those pages are enclosed with this Case Evaluation Report.
This lady was painting a fence in December 2004. It was unstable, jerked her injuring her back. The Neurologist examined her two weeks later. Dr. W found a completely normal neurological examination, including her legs.
By April 2005 she had a different problem. The previous month she hit her head entering a car and began to have numbness and tingling on the left side of her body. The physical examination again was normal. The MRI of her brain was consistent with a mild contusion (bruise). He ordered a number of blood tests and ruled out lupus, syphilis, and some other chronic diseases.
In April she had previously visited the Emergency Room complaining of weakness of her right knee and a burning sensation in her left thigh and down her leg. Her physical examination, including of her legs, was negative. There was no swelling or local calf pain noted, and as I noted, the examination the same month also was negative.
Because her symptoms did not resolve, Dr. W properly ordered a MRI of her cervical (neck) spine. This revealed some spinal cord swelling that could be consistent with multiple sclerosis or diffuse spinal cord inflammation called transverse myelitis. He began her on steroids to try to control the swelling. She had some improvement in her symptoms and in a repeat MRI, by August 2005.
By September 2005 she developed abnormal reflexes and was to be sent to J Hospital and apparently was treated at P Hospital for two weeks in September 2005. I have not seen any of their records, not even the admitting history and physical, consultation reports and the discharge summary. Multiple studies for the diagnosis of multiple sclerosis (MS), including a spinal tap and MRI of her brain were negative for this condition.
By November 2005 her presumptive diagnosis was transverse myelitis. During every visit her legs were examined by testing for reflexes. No swelling or calf pain was ever found. Its presence would have been obvious. During these months she developed a significant anemia which was never fully evaluated.
She was maintained on oral steroids to try to control her alleged transverse myelitis from an unknown cause and medication to try to reduce her periodic leg spasms. She did not have any persistent leg muscle pain or other findings with thrombophlebitis (blood clot inflammation within leg veins).
By February 2006 she had “obvious right hemi-ataxia” (weakness and abnormal motion) on her right side but she always was able to walk. She was not bed ridden. Persistent immobility in bed does raise the risk of blood clot formation in leg veins. She did not appear, per the records, to be at a significantly higher risk for this problem.
On 2/23/2006 she was seen in the Emergency Room at RL Hospital because her weakness and numbness from her diagnosed transverse myelitis had increased. There was weakness of all her extremities, especially her right side. No leg swelling or pain was noted. She was supposed to be admitted to the hospital by Dr. M (? spelling in record unclear), but I have no in hospital records other than the admitting history and physical which showed only slight weakness (strength was 4/5 on right upper and lower extremities), and no other leg problems noted by this doctor or Dr. W. She was sent home after three days of a higher dose of injectable steroids. On discharge she “had significantly increased strength in both extremities”.
On March 28 he saw her in his office and noted: “She still has the right hemi-paresis but she is able to ambulate without assistance.” All that is strong evidence against a significant risk for thrombophlebitis and against having that painful leg vein clot condition.
I have no further medical information concerning her until the death certificate for April 15, 2006 which noted that there was an autopsy performed (for which I have not seen any records) and documented that she died from a pulmonary embolism at age 43.
A pulmonary embolism is a blood clot that blocks the heart lung blood flow circuit. The pulmonary artery supplies all the un-oxygenated blood from the entire body that has been pumped by the right ventricle through the pulmonary artery into the lungs. There the blood is oxygenated. There the blood is oxygenated and flows into the left side of the heart where the left ventricle pumps it all under higher blood pressure into all the arteries of the body, and eventually to all its trillion of cells.
In almost all circumstances, these blood clots arise in the deep leg veins, break loose and travel via the veins into the heart lung circuit. Minor ones often cause chest pain. A single very large clot or a number of clots can cause death by blocking this heart lung blood flow like a cork.
Unlike thrombophlebitis which usually causes significant leg pain and swelling (none of which she had), silent blood clots that are present without any signs or symptoms of inflammation (phlebothrombosis) are able to go unrecognized and cause death by massive pulmonary embolism.
Patients with leg fractures, hip operations and otherwise being maintained at prolonged bed rest are at very high risk for this condition. Therefore, these patients are maintained on air pump pressure leg bandages and an injectable blood thinner (Heparin), intended to prevent leg vein blood clot formation and lower the risk of pulmonary embolism. She did not have these risk factors, and therefore did not need this extraordinary therapy.
Without these risks factors or any signs of chest pain or leg pain (continuous) or swelling, she received reasonable care for her condition and her death by pulmonary embolism was not from any departures of the standards of care for any misdiagnosed thrombophlebitis or needed prophylactic anticoagulation (blood thinners).
I did note that during her last hospitalization she had a few blood coagulation tests performed. The prothrombin time and its related INR tests were basically normal (the PT test was just minimally high, meaning the blood would clot slightly less). The PTT (partial thromboplastin time) test was slightly low at 18.8 versus the normal range of 25 to 31 seconds. This would mean that her blood had a slight propensity to clot faster. However, without any blood clot signs or symptoms, most physicians would not do anything further. She also had an order for the “heparin lock”, which is the insertion of a needle into a vein and the use of the blood thinner (anticoagulant) heparin to be used in a concentrated form to keep the intravenous needle from clotting. But that amount of heparin is very little, and should not affect the PTT blood test. Further more, it appears that the blood test was drawn at 1410, probably before the hep-lock was begun. That timing should be resolved by the Nurses notes which I have not seen. Possibly the lab technician drew the PTT through the heparin contaminated needle.
I mention the above because what I will be discussing next, and that may be related to an increased clotting ability of her blood, in addition to her spinal cord nerve damage.
However, there is a potential serious matter of liability in this case. On March 10, 2006 a Naturopathic Doctor: “C”, ND (not MD) ordered and obtained the testing of this patient’s hair for “Elemental Analysis” at the GR Diagnostic Lab. This test was completed on March 16, 2006. It revealed very high (toxic) levels of antimony, arsenic and lead. The elevated level of gadolinium would not be toxic and would be from the contrast dye used in the MRI examination.
Lead is a nerve (neuron) poison and causes brain and spinal cord injury. It may have been the causation of her so-called transverse myelitis, and anemia (which was never properly evaluated).
Hair analysis is somewhat controversial, but is an accurate method for determining long-term poisoning since the hair follicles produce the hair from body substances. The levels for antimony, arsenic and lead are very, very high.
I noted that her initial problem (injury) occurred when she was painting. Was that her profession? Lead based paint was banned in the United States in 1978 because it contained almost 50% lead by weigh and is poisonous. Many older houses and buildings were painted with lead and its scrapings cause lead dust to be inhaled at high levels.
Was her water supply contaminated with these heavy metals? Are her family members at risk? Have they been tested for these toxic heavy metals? Who is responsible for her poisoning?
The problem is causation with death from pulmonary embolism. I am not aware of any causation, but a Specialist in Hematology and one in Public Heath matters maybe able to give you a correlation of causation. And depending on the source of contamination, you may very well have a huge potential class action lawsuit option.
I would suggest that you contact Dr. C to obtain her records and assistance in this matter, too.
It is important to find out if they saved any of her blood from her autopsy. If so, have her blood tested for lead and arsenic. Our office will provide the Hematologist Expert should you decide to look into correlation of lead poisoning.
Based upon the information in the records received it would appear that the above issues represent viable avenues of pursuit in this case and the potential to obtain supportive Expert Witness opinions supporting the issues that pertain to a possible class action law suit may exist, although no guarantees to that effect can be made.
We continue to remain available to assist you in this case and have the Expert Witness specialties you require for this case.
Thank you for allowing the Medical Review Foundation, Inc. to be of assistance in reviewing this interesting case.
Our office awaits your written instructions.
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Transient Ischemic Attacks Went Untreated, Resulting in a Severe Stroke and Hospitalization.
The "timeline of this patient" refers to her husband informing Dr. #1 that "she was also having a problem with moving her right arm and holding on to things." Depending on how that occurred, this would be consistent with what is called a transient ischemic attack, or a mini stroke that clears. In a patient of age 70 with a history of hypertension, in my opinion, investigational studies are required. This usually would consist of a carotid Doppler ultrasound blood flow study, which, in my opinion, in her case, based upon subsequent studies, would have shown significant impairment of blood flow through the left internal carotid artery. The left and right carotid arteries bring 80% of the blood to the brain, the rest being supplied through the vertebral arteries. There is some cross communication at the base of the brain called the circle of Willis that if the branches from that become blocked, such as in her case, the middle cerebral artery, there will be death of brain substance, which is a stroke (cerebrovascular accident; CVA).
Treating a patient with hypertension certainly does meet the standard of care. When there is evidence consistent with a transient ischemic attack, then the use of aspirin as well as the drug Persantine would meet the standard of care, and to some degree, would reduce the risk of stroke formation. There is a slight increased risk of hemorrhage within the brain if there is a hemorrhagic stroke, but the majority of physicians, in my opinion, would begin therapy with these medications as well as investigative studies. If the carotid ultrasound study was abnormal, as it most likely would have been in her case, then an invasive carotid angiogram (artery x-ray dye contrast study) would be the next study to take place, and then operative intervention sometimes is justified, depending upon the findings on that study.
Because of a car accident and a back injury, the patient had been in chronic pain, and was hospitalized at the Rehabilitation Hospital for care for her back. On admission to the hospital on September 2, her blood pressure was normal at 138/80. Neurologically, she was perfectly normal, and on her neck examination, they noted "no carotid bruits." This means there was no abnormal whistling sound of blood through a narrowed artery, but that does not mean there was not further narrowing in that blood vessel, including higher up toward the brain direction, as I mentioned above.
If her physicians were advised of the transient weakness involving her right side, including her arm, then in my opinion, there is an affirmative duty to investigate and use preventive drug therapy, as I have described above.
During her hospital stay, the patient was receiving occupational and physical therapy, and in fact was doing well until the evening at approximately 7 or 9 p.m. on September 7th when she developed evidence of an acute stroke with paralysis involving her right arm and most of her right side, as well as difficulty in speaking and swallowing. The left side of the brain controls the right side of the body.
That night, just prior to midnight, the patient was transferred to the Intensive Care Unit. The next morning, September 8, a CAT scan of the brain was done without contrast at 7:49 a.m., and this showed "acute infarct in the anterior distribution of the left middle cerebral artery." The findings were discussed with Dr. #2, and the patient was begun on one-half of an aspirin per day, as well as the blood thinning medication Lovenox (which is related to heparin) on a prophylactic rather than therapeutic dose. Because of the dense infarction in the brain, the neurologist was concerned that if they used the high-dose heparin therapy, there would be risk of hemorrhage. This is a reasonable decision.
Currently, some university medical centers in a stroke that is thrombotic (blood clot forming) rather than hemorrhagic would use the blood clot dissolving drug, TPA (tissue plasminogen activator), but even today that does not meet the standard of care. It potentially exceeds the standard of care, and there was significant risk of converting even a thrombotic stroke into an hemorrhagic stroke.
For a heart attack, the indications are well documented. The benefits generally outweigh the risks, but for a stroke, this is still in an experimental level of therapy, and there are significant risks of hemorrhage within the brain.
Other than the aspirin and Lovenox therapy, simply a matter of passage of time is what takes place in a hospital setting. The patient was receiving food through a nasal gastric tube, then eventually a tube was sewn into the stomach. She was then transferred into a nursing home. According to the nursing records, the patient did make some slow improvement over time, but was significantly debilitated and presently, according to the timeline, is bedridden at home with significant neurologic impairment secondary to the stroke that occurred that evening.
Other than my concerns for the failure to further investigate the findings consistent with transient ischemic attacks as noted in the "timeline," and therapy at that stage may have prevented the stroke, I do not find departures from the accepted standard of care during the hospital stay following the development of the stroke and the therapy that occurred thereafter.
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Post-operative patient develops neurological symptoms, and has delay in diagnosis and therapy of Guillain-Barre Syndrome.
The patient was a thirty-three year old female who was otherwise healthy when she presented to the Emergency Ward of Hospital #1 with complaints that included pains in her chest, back, and legs. She was allegedly diagnosed with a urinary tract infection and was discharged home.
Details of this Emergency Ward visit were missing from the materials that I reviewed and might be useful to this case. For example, leg pain would be a very unusual symptom to accompany a urinary tract infection and might well have represented the initial symptom of Guillain-Barre Syndrome. These records, in my opinion, should be further pursued.
On April 14, the patient was seen by Dr. #1 for worsening abdominal discomfort and she underwent an appropriate office work-up that included an abdominal CT scan which revealed gallstones. In this setting, Dr. #1 opted to admit the patient to Hospital #1 for eventual cholecystectomy. On April 15 she underwent a laparoscopic cholecystectomy.
The patient's postoperative course was complicated by bladder fullness which necessitated the use of an indwelling catheter. In addition, Dr. #1's discharge summary documented that the patient also suffered from tingling around her eyes and finger numbness. The extent of the work-up that was undertaken for these neurologic symptoms was that Dr. #1 ordered a calcium level that was normal.
It can be stated, within a reasonable degree of medical certainty, that the standard of care for a postoperative 33 year old cholecystectomy patient who can not void and has additional neurologic symptoms including tingling and numbness, required the consultation of a Neurologist to exclude potentially life-endangering conditions such as Multiple Sclerosis and Guillain-Barre Syndrome.
The failure to consult a Neurologist, as early as April 16 (and possibly even earlier) represented a deviation from existing standards that, more likely than not, adversely impacted on this patient's prognosis.
Guillain-Barre Syndrome is a neurologic disorder of unclear cause. It is known to be associated with a number of other disorders and is most often postinfectious in nature, occuring, for example, in the aftermath of an upper respiratory tract viral infection such as the flu. Guillain-Barre is also known to be associated with patients who have undergone a variety of surgical procedures, and as such, should have been suspected here. In Guillain-Barre Syndrome, peripheral nerves are damaged, presumably by the body's production of antibodies that are directed against these nerve fibers. Medications and procedures that are known to alter the production rate or removal of these antibodies such as immunoglobulins or plasmapheresis are the mainstay of therapy for this condition and have their biggest benefit when begun early in the course of the illness (references available upon request). Generally, plasmapheresis is the preferred therapy over immunoglobulin therapy but was unable to be used here due to the delay in diagnosis and initiation.
Dr. #1's discharge summary suggests that Dr. #2 was also involved with the medical management of the patient on or about April 16 but I am unable to find this documentation. Similarly, there is a reference to an office visit with Dr. #2 on April 18 in which the patient had allegedly experienced walking difficulty, but I am similarly unable to find documentation of this outpatient evaluation.
On April 20 the patient sustained a fall, presumably due to leg weakness and was re-admitted to the Hospital #1 to the service of Dr. #2. The Emergency Ward Physician who cared for her was Dr. #3. Dr. #3 obtained routine lab tests that included a serum sodium of 121 mg/dl which is markedly abnormal, but not low enough to account for all of this patient's neurologic difficulties such as the bladder dysfunction. Dr. #4 cared for this patient on April 21 and ordered a neurology consultation, a CT of the spine and other studies that were within the accepted standards of care.
The Neurologist, Dr. #5 evaluated this patient on April 21 and correctly established an excellent differential diagnosis that included Guillain-Barre Syndrome. A spinal tap that was performed revealed an elevated protein level, consistent with the diagnosis of Guillain-Barre Disease. Also, Guillain-Barre Syndrome is known to cause abnormalities of the patient's electrolytes, such as the serum sodium, which was otherwise very difficult to explain in this young, otherwise previously healthy patient.
However, despite these considerations, and the fact that untreated Guillain-Barre Disease can lead to rapid neurologic, respiratory and other serious complications, no specific therapy for this disease appears to have been begun while at the Hospital #1. However, other supportive measures such as corrective efforts to raise the patient's serum sodium were appropriately undertaken although the specific cause for this unusual electrolyte disturbance was overlooked.
On April 24 the patient was transferred to the Hospital #2 where immunoglobulin therapy was ordered by Dr. #6. Immunoglobulin is one of the treatments that are specifically used to treat Guillain-Barre Syndrome, but, as mentioned, is generally regarded as less effective than plasmapheresis and is further rendered less beneficial when begun after a delay of over one week.
Dr. #6's management of the patient appears to have been entirely within acceptable standards of care and included a five day course of immunoglobulin therapy, supportive inpatient care and close outpatient follow-up including physical therapy and pain control. It should be appreciated that, despite these measures, the patient had persistent pain and weakness on the last note from Dr. #6 on October 21, some six months following the initial diagnosis. The long-term progress of this patient's condition is unknown from the available records.
In summary, the patient underwent a laparoscopic cholecystectomy on April 15. Her postoperative course was complicated by urinary voiding difficulties and a variety of neurologic complaints including tingling and numbness for which an inadequate work-up was undertaken by Dr. #1. There were also apparent outpatient visits that suggest that additional delays in diagnosis and treatment occurred on behalf of Dr. #2 but these records are unavailable.
Clearly Dr. #1 was negligent in his failure to timely diagnose, treat and obtain neurologic consultation for this patient. Similarly, upon readmission, to Hospital #1, additional delays in diagnosis and treatment occurred on behalf of Drs. #2, #3, #4 and the Neurologist, Dr. #5 as well as possibly additional caretakers.
The Hospital, itself, must be held responsible for the deviations that occurred among its Staff. These delays contributed significantly to the prolonged pain and neurologic disabilities that this patient continued to experience for a period of over six months.
Additional input from a Neurologist may be particularly useful to establish the relationship that the delay in initiation of treatment had in the development and severity of this patient's symptoms. It may also be very beneficial to obtain a more complete set of the medical records since a number of seemingly important entries were unavailable.
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