A Medicolegal Examination into the Death of Bruce Lee: A Case Study

A Medicolegal Examination into the Death of Bruce Lee:
A Case Study


By
Dr. Craig M. Pradarelli, BA, BSc, MD




Abstract


This article will examine the death of Bruce Lee through the eyes of an experienced investigator, currently a fourth-year medical student.  A review of all publicly available information relative to the health and medical history of Mr. Lee was made.  A history and physical of Mr. Lee is presented with modifications as if he were being treated by a physician at the time of his death.  From the information available, conclusions can be made with respect for his death due to Sudden Unexpected Death in Epilepsy.


Key Words: Bruce Lee, Sudden Unexpected Death in Epilepsy


Published in The Forensic Examiner®-January 2016



Bruce Lee was one of the most innovative and well-known martial artists of the 20th century.  He died on July 20, 1973 at the age of 32, which shocked and stunned the martial arts world.  All the pictures of Bruce Lee taken then showed one of the most well-defined physiques of that time, and since.  Understandably, there was a great deal of disbelief that a person with his physique could have died a natural death.  The fires of this disbelief were fueled by inaccurate information released from his management team regarding the location of his death.  Grandiose rumors as to the cause of Bruce Lee’s death began to circulate in the press as well as among the population at large.  The rumors persist to this day.


The mystery surrounding Bruce Lee’s death years later was perpetuated by statements made by people who should have been more responsible with their speech.  This includes pioneer karate businessman Ed Parker, who stated, “Many of us do not know the inner thinking and secrets of the Chinese herbalists.  They have herbs for medicine and they have ones we’ve never heard of for poison.  I believe it was foul play that killed Bruce Lee” (Bleecker, 1996).


Although the final autopsy was never released to the public and requests for it have been declined, those in possession of it have been kind enough to share portions of it with the author.  Aside from the parts of the autopsy that have been shared, there is enough publicly available information to arrive at a fairly accurate postmortem diagnosis of the cause of death in Mr. Lee.  It should be noted that while academic medicine is very precise, the actual practice of medicine in many instances can only provide an approximation or a series of possibilities as to cause of death.


As such, the precise cause of the death may never be known or made public. However, recently published research discusses a syndrome, Sudden Unexpected Death in Epilepsy, which is consistent with facts surrounding the death of Bruce Lee.  While Sudden Unexpected Death in Epilepsy is currently acknowledged as a medical phenomenon, it had its distracters in the 70s and 80s, and this added to the confusion surrounding his death.


At the time of his death, neither of the insurance companies that had life insurance policies were satisfied with the explanation of his death.  Decades later, one of Bruce Lee’s close friends, Tom Bleecker, wrote a book exploring his death.  He commented, “In another cabinet one file stood out among all the others: ‘BRUCE’S AUTOPSY REPORT.’  I sat down and read it.  By the time I had finished reading it for the third time, I felt sick.  Something was wrong” (Bleecker, 1996).


In the 35 years since the death of Bruce Lee, statements have been made running the entire range of possibilities and speculation.  What is clear is that the cause of death was cerebral edema.  Cerebral edema can be caused by a multitude of drugs, chemicals, and disease processes and is a situation where water accumulates in the brain and causes dysfunction as the pressure builds, due to the skull’s remaining intact.  This dysfunction causes death if not treated properly.  In this case, cerebral edema is not up for debate as being the cause of death, but rather, the cause of the cerebral edema is.


In those same 35 years that the mystery surrounding the death has been perpetuated, medical and forensic science have advanced.  As such, a medical history and physical of Bruce Lee has been put together using the available sources, including autopsy information, statements relative to the death scene, and a list of different diagnoses that will lead to the most probable cause of death in light of current medical literature.  It is not the aim of this article to assign a criminal or civil liability for the death of Bruce Lee to a specific individual.


Before going further into the medical history and death investigation of Mr. Lee, it is essential to describe the mechanism of cerebral edema.  Cerebral edema has its origins in cellular physiology.  The mechanism responsible for keeping the proper amount of water in the cell is known as the sodium-potassium pump.  Sodium is an extracellular ion, meaning that it normally finds its home outside of the cell, in this case the brain cell, also named a neuron.  In order for the neuron to function, sodium rushes into the cell and causes it to “fire” or send electrical and chemical messages to the next neuron or target organ.


When sodium enters a cell, water follows.  There is an axiom in physiology that where sodium goes, water follows (Shastry, 2004).  After the sodium and water have entered the cell, it is removed by the action of a mechanism known as the sodium potassium pump.  This mechanism keeps the cell in proper functioning order.  When this mechanism fails, there will be an increase in the amount of water in each cell.  Due to the fact that the neurons are encased within the skull, the swelling of these cells begins to put pressure on the rest of the brain, causing there to be a reduction in the proper amount of blood entering the brain and bringing along with it oxygen while removing waste products produced by the brain cells.  Unless this process is halted or reversed, damage will occur to the portions of the brain that regulate and control breathing and heart rate.  Left unchecked, death will ensue in short form.


The question in the case of Bruce Lee is what caused the inhibition of the sodium potassium pump leading to cerebral edema.


Method


In order to properly study the death of Bruce Lee, a variety of material was reviewed with respect to his medical treatment and medical history, as well as to what extent possible results of a physical examination that would have been available at the time.  These results were then placed into the form of a standard medical history and physical.  Also, as best as can be reconstructed, a death scene evaluation was produced.  From these results, a list of differential diagnoses was constructed to yield the most probable cause of the inhibition of the sodium potassium pump.


Interviews with three of Bruce Lee’s treating physicians were reviewed as well as the book Unsettled Matters (Bleecker, 1996), and also interviews with those who were in contact with both Mr. Lee (Edmond K. Parker, personal communication, 1986; Tom Bleecker, personal communication, 2005 and 2008) and other members of the martial arts community at the time.


Identifying Data


Lee, Bruce 32 years old, Asian, Male, 5’7”


Chief Complaint:


Headache


History of Present Illness:


On July 20, 1973, Mr. Lee reported that he had a headache this evening and laid down to rest.  A few hours later, he was unable to be aroused for a dinner engagement; a physician was summoned, who spent 10 minutes attempting to revive him.  He was transported to the hospital but arrived dead on arrival.


Past Medical History:



Past Surgical History:


Auxiliary Sweat Glands removed December 1972


Allergies:


No known allergies


Family History:


Mother:

Grace Lee Alzheimer’s disease


Father:

Hoi-Cheun Lee (Died in 1965 at 64 years old)


Son:

Brandon Bruce Lee, killed in work-related injury on March 31, 1993


Daughter:

Shannon Lee


Brothers:

Robert Lee

Peter Lee


Sisters:

Agnes Lee

Phoebe Lee B. 1938


Social History:


Married, two children, long-term daily Cannabis use, martial arts instructor and lifelong movie actor


Avid martial artist, involved in many combative episodes


Has some college education with a major in philosophy, author of several books


Alcohol use


Review of Systems:


General:

Weight loss over last 6 weeks


Skin:

Darkened freckles, growing darker during past 3 weeks


Head:

Frequent Headaches


Eyes:


Ears:


Nose:


Mouth:


Respiratory:


Cardiovascular:


Gastrointestinal:

Nausea and Vomiting


Genitourinary:

Undescended testicle


Endocrine:


Musculoskeletal:

Short Leg, Chronic back pain, Body fat less than 1%. Extremely well developed musculature


Skin and Lymphatic:

Darkening of skin


Neuropsychiatric:

Reported incidences of violent outbursts, and developing paranoia, stress


Physical Examination


General Appearance:

Has the physical appearance of an extremely well-developed musculature. Last medical examination proclaimed him to be in the physical condition of someone 10 years younger than his stated age.


Vital signs:


Skin:


Lymph nodes:


Head:


Eyes:


Mouth and Throat:


Neck:


Chest:


Heart:


Breast:


Abdomen:


Genitourinary:

Undescended testicle


Extremities:

One leg shorter than the other


Rectal Examination:


Neurological:

Loss of Consciousness


Cranial Nerve Examination


No abnormalities noted


Labs



Assessment:


Mr. Lee is in a very poor state of health.  His body fat is in the percentage of someone suffering from anorexia nervosa.  The previous examining physician indicated that he had the body of someone in his 20s, which may have appeared to be a sign of good health, but in retrospect may be interpreted as a sign of an unhealthy individual.  It appears that he is having an ongoing organic brain syndrome manifesting itself in the form of paranoia, which he self-medicated with cannabis, as well as having violent outbursts.  He was noncompliant with this Dilantin at the time of this incident as no metabolites were reported.  There seems to be some disruption of the sodium/potassium pump in the cerebral tissues causing two episodes of cerebral edema, enough to cause unconsciousness and death.  The cause of the disruption of the sodium potassium pump appears to be an underlying pathology in this matter.


Plan:


Determine the cause of the inhibition of the sodium potassium pump


Increase nutrition to bring body fat into normal range


Monitor closely for neurological deficits


Continue Dilantin


Manitol as needed to control swelling


Neuropsychological Assessment


Differential Diagnosis:


  1. Subdural Hematoma
  2. Epidural Hematoma
  3. Subarachnoid Hematoma
  4. Anaphylactic Shock
  5. Dim Mak
  6. Poisoning
  7. Addison’s Disease
  8. Lactic Acidosis
  9. San Gong (Too much training)
  10. Sudden Unexplained Death in Epilepsy

Death Scene Evaluation:


Mr. Lee was found by Betty Tai Ping in her bed after he went there to rest for a reported headache.  She admitted to giving him a tablet of Equagesic, which is Meprobamate and aspirin.  She was unable to arouse him after going to check on him.  There was a series of phone calls between Betty and Raymond Chow before she phoned her physician, who came to the scene and found him to be a pulseless nonbreather.  Dr. Eugene Chiu related that Mr. Lee was found in a bedroom, in a supine position.  He noted that he was nicely dressed and that there appeared to be no signs of a struggle.  He related that he appeared to be very relaxed.


Dr. Eugene Chiu attempted external cardiac massage, with no mention of establishing an airway.  An ambulance was called.  Later, another one of Mr. Lee’s physicians was called by a “house officer” at the hospital taking his advice on the matter.  It was indicated that Mr. Lee was clearly deceased.  The house officer was advised to refer the matter to those in the administration of the hospital.  Dr. Eugene Chiu indicated that he did not prescribe Equagesic to Miss Tai Ping.


Autopsy:


As the entire autopsy protocol has not been made available, the released portions are contained herein: all organs, with the exception of the lungs and the brain, were reported to be normal.  Special inquiry had been made with respect to the adrenal glands due to suggestion by Tom Bleecker that Bruce Lee had been using steroids.


External Examination:

No evidence of trauma


Oropharynx:

Clear and normal, no evidence of vocal cord swelling


Skull:

Intact


Brain:

1, 575 grams (normal 1,400 grams)


Severe cerebral edema


The blood vessels of the brain intact and unblocked


Lungs:

The covering of the lungs showed a degree of minor hemorrhaging and moderate congestion


Some fluid in the lungs


Internal congestion of the vessels


No evidence of pneumonia


In some areas, blood had burst through the vessels and entered the air space of the lungs


Heart:

Normal


Spleen:

Normal


Liver:

Normal


Kidneys:

Normal


Adrenals:

Normal.  “There is no evidence of destruction to adrenal glands”


Labs:

Marijuana, positive


Dilantin, negative


Other illicit Substances, negative


Discussion:


This case is admittedly a complex and perplexing one.  Thirty-five years later, and the controversy remains.  The case was subject to civil litigation when the death occurred.


The insurance companies must have been unhappy.


While the death by misadventure ruling assumes that Bruce Lee’s death was caused by a reaction to the Equagesic table that he took to relieve his headache, it ignores the fact that the mechanism that caused his death may have already been in place and caused the headache as well as his seeking relief from the pain of that headache with the Equagesic tablet, and then resting in Miss Tai Ping’s bed.


Seen in this light, a different series of events unfolds.  What becomes evident is that a diagnosed epileptic who had a near fatal seizure six weeks before is found dead in a bed where he went to escape pain.


It would appear that Mr. Lee may have succumbed to the syndrome Sudden Unexpected Death in Epilepsy, as many of the factors described in the literature about this syndrome are consistent with the events preceding Mr. Lee’s death, and the manner of his death.


Sudden Unexpected Death in Epilepsy (SUDEP) is a medical phenomenon that has been described as “sudden, unexpected, witnessed or unwitnessed, nontraumatic and nondrowning death in patients with epilepsy with or without evidence of a seizure and excluding documented Status epilepticus, in which post mortem examination does not reveal a (structural or toxicological) cause of death” (Nashef, 1998).  There are problems with this definition, as many who die of this disease do not undergo autopsy.


The risk factors for SUDEP are “youth, male gender, remote symptomatic epilepsy, structural findings on neuropathology, severe epilepsy, unwitnessed seizures, alcohol abuse, abnormal eletroencephalograms (EEGs) with epileptiform changes and greater variations in mental disability, psychotropic medications, African American race, lack of adherence to treatment, abrupt medication changes, and low AED (antiepileptic drug) levels” (Nashef, 2008).


First, it must be established that Mr. Lee was an epileptic.  There is sufficient evidence to support the fact that Mr. Lee was, in fact, an epileptic.  That evidence is found in the interview of Chow Fook Wing, a sound mixer who sad, “[We] just broke for lunch, when shouting broke out.  Bruce was lying in front of the toilet.  His mouth chattering as if he was experiencing and epileptic fit.”  The person who is identified as his teacher, Wong Shum Leung, readily admits that Bruce had epilepsy as a child.


Other evidence of epilepsy is provided in Unsettled Matters,where Mr. Bleecker quotes physicians examining Bruce Lee as saying, “Based on the extensive battery of medical tests conducted on May 25, 1973, Dr. Karpman found Bruce to be in sound physical health, and Dr. Reisbord concluded that, other than a manageable seizure disorder, there really wasn’t anything wrong with Lee” (Bleecker, 1996).  One must read between the lines to obtain a diagnosis with respect to the May 25 examination.  It clearly reads that Bruce Lee has a “seizure disorder.”


Dr. Langford who is quoted in Unsettled Matters and speaks for himself in Death by Misadventure mentions that Bruce Lee was “alternating flaccidly” and that “his neck seemed rigid part of the time.”  These symptoms are suggestive of a tonic clonic seizure.  Further, the following day, he was prescribed Valium, which is a treatment for epilepsy.


The second matter to consider is the relationship of epilepsy to cerebral edema. There have been several studies published in recent years that demonstrate, via methods not available at the time of Bruce Lee’s death (MRI, CT), a relationship between epilepsy and cerebral edema.  Review of the medical literature reveals many instances of cerebral edema in epilepsy.


Jeong-Ah Kim and associates in 2001 found that “the initial MR images revealed focally increased T2 signal intensity, swelling, and increased volume of the involved cortical gyrus in all eight patients.  The lesions were located in the cortical gray matter or subcorticol white matter in seven patients and at the right hippocampus in one” (Kim et al., 2001) in epileptic patients.


Nolte reported a case in 2004 very similar to that of Bruce Lee’s in which a previously healthy 23-year-old male was admitted to the emergency room with convulsions.  Resuscitative efforts were unsuccessful.  Autopsy showed “general brain edema” as well as other neuropathology, which were either not looked for or discussed in the Lee autopsy material (Nolte, 2004).


One other study published more recently related, “Based on histological findings showing brain edema without specific abnormal findings (malignancy, inflammation etc), we concluded that… the edema [was] induced by the seizure attack” (Misumi, 2006).


Interestingly, while each of the three studies cited supports the position that epilepsy is associated with cerebral edema, the technology that was used in two of these studies (MRI) was not available at the time of death of Bruce Lee, thus not allowing for an empirical connection to be made between epilepsy and cerebral edema at the time of Bruce Lee’s death.  Additionally, the Kim study as well as the Misumi study were performed on an Asian population which, if properly controlled, would make them more applicable to Bruce Lee than those from another demographic.


One further factor needs to be examined with respect to the brain edema in Mr. Lee: the correlation of lactic acid.  There have been studies that correlate lactic acid with the cerebral edema.  K. Lipka and H.H. Bulow demonstrated that “Lactic acidosis is a common cause of metabolic acidosis and is usually connected with high mortality.”  Continuing, they found that “changes in the level of lactate and pH can also be seen after generalized epileptic attacks, due to local muscle hypoxia during the seizures.”  This problem could have been conceivably been exacerbated in Mr. Lee due to his excessive training schedule as well as the use of “the electric shock stimulator and its entanglement of wires and electrodes Bruce used to affix to his muscles so he could exercise even while he slept” (Bleecker, 1996).  The use of this device has been confirmed by other serious martial artists (Robert Penny, 2008).  The use of this device as well as his rigorous training schedule could have raised the lactic acid content of his body.  If there was a metabolic acidosis due to a seizure at the time Bruce Lee was at Betty Tai Ping’s apartment, then this increase in lactic acid caused by his exercise and electronic stimulator could have inhibited the sodium potassium pump.


There is recent literature (Richter, 2007) that suggests that San Gong, over training or excess physical exercise, can precipitate an experience such as was experienced by Bruce Lee during the May incident.  The Richter article refers to a previously healthy triathlete who, upon completion of the event “presented with somnolence and convulsion… radiological examination revealed pulmonary as well as cerebral edema… She had to be intubated, mechanically ventilated…  After treatment with Furosemide recovery occurred (Richter, 2007).  While the mechanical aspects of the incident reported in the Richter study are very consistent with the May incident of Mr. Lee, special attention should be paid to the fact that in each case, recovery occurred following the administration of a diuretic: Manitol in Mr. Lee’s case and Furosemide in Richter’s case.


While review of the above material suggests that Bruce was, in fact, an epileptic, there are other factors to consider in the diagnosis of SUDEP.  A major factor found in the research on SUDEP deaths is noncompliance with medication.  Mr. Lee was prescribed Dilantin at the time of the May seizure.  The public portions of his autopsy indicate that there was no Dilantin found in his system.  This suggests noncompliance with his medication and scores as a factor in making SUDEP more likely.


Dilantin, also known as Phenyton, is a drug used in the treatment of epilepsy.  Its use in this case needs some exploration.  There is a caution in a pharmacology book used to train physicians in the discussion of phenytoin that reads, “Antiepileptic therapy should for tonic clonic seizures should never be terminated abrupty; otherwise seizures may result” (Howland, 2006).


Dilantin has a half-life of 24 hours, therefore it can be extrapolated that Mr. Lee had discontinued his Dilantin therapy at the very least three to four days before his death.  There was also no discussion of Valium (Diazepam) found at the time of his autopsy.  Diazapam also has a fairly long half-life.


Interestingly, Dr. Peter Wu, a neurosurgeon who treated Mr. Lee at the time of the May seizure, was under the impression that Lee thought he was invincible.  This over-confidence may have had an influence on his noncompliance with the Dilantin.  This sentiment is echoed by Dr. Jeane Haining, who performed her doctoral dissertation on medication compliance, and stated that “athletes would be less inclined to remain compliant to such drugs due to the sedating effects of the drug which would impair their athletic performance” (Haining, 2008).  Continuing, she related a similar situation where individuals who are bipolar will remove themselves from their Lithium treatments under the misunderstanding that they are feeling well, so they do not need it.


An inference can be made that those who become noncompliant with their medications after a period of successful treatment may feel that the drug functions in the same way as an antibiotic functions.  Those who are noncompliant with their medications may misunderstand the drugs’ mechanisms.  They may find that the drug has cured the condition, not understanding that these drugs are for maintenance of a disorder and do not cure it.  Dr. Wu’s opinion reflects this position.


Two further points must be addressed with respect to the medications that were involved.  The mechanism of action of Phenytoin is extremely important to this case. “Phenytoin blocks the voltage-gated sodium channels by selectively binding to the channel in an inactive state and slowing its rate of recovery.  Thus, depolarization and frequently firing neurons are particularly sensitive to the blockage” (Howland, 2006).  As Phenytoin slows the entry of Sodium ions into the neurons, it also slows the entry of water into the neurons as well.  Thus, if Mr. Lee were to have remained on his prescribed Phenytoin, it would have reduced the chance of his suffering a seizure on the date of his death, as well as inhibited the progression of the cerebral edema that all parties involved agree was the cause of his death.


The officials involved in this case were under the impression that the Equagesic table, the active ingredient being Meprobamate, was influential in his death.  Still, it is unlikely that this table could have caused the edema or a seizure.  The medical literature does not support Meprobamate causing similar symptoms.  Most importantly, Meprobamate was replaced by a class of drugs known as benzodiazepines, of which Valium (Diazepam) is a member.  Although the mechanism of action of Meprobamate is not known, it seems unlikely that a drug given to relax muscles and reduce anxiety would impact this particular case in any way but to reduce the symptoms of a seizure, as Meprobamate has been demonstrated to have an anti-seizure effect.  As mentioned before, it was taken to alleviate symptoms that were already in place at the time of administration.


It would be remiss to not address the fact that on both the May incident as well as the date of his death, marijuana was found in his system.  The following quotes mentioned at the time of his death address the significance of the marijuana.  “The first was that of government chemist Dr. Lam King-leung, who testified that only a small amount of marijuana had been found in Lee’s stomach and small intestine.  The second, and more critical testimony, was that the Professor Ronald Teare of London University’s Forensic Medicine Department, who had flown to Hong Kong specifically to give his expert opinion that he considered the marijuana found in Lee’s body, ‘about as significant as if I had been told Lee had taken a cut of tea or coffee’” (Bleecker, 1996).  Current research is indecisive as to the effects of marijuana on epilepsy, but tends to show an inclination toward reduction in seizures.  “Anecdotal reports describe either improved or worsened seizure control temporarily associated with marijuana use… In a placebo controlled study of 16 epileptics refractory to other drugs, cannabidol acutely exacerbated EEG abnormalities but not behavioral seizures; after several months, however, seven of eight patients receiving cannabidol were seizure-free compared to one of eight controls” (Cunha et al, 1980).  The above suggests that if anything, the marijuana in Bruce Lee’s system may have had a protective effect and was not in any way related to the cause of his death.


While the marijuana itself may have had a protective effect in seizure occurrence, Dr. Wu believed that Bruce Lee may have had sensitivity to marijuana.  This sensitivity may have induced the vomiting that was reported on the May event.  While there is not enough information to determine just exactly how much emesis was taking place in Mr. Lee’s life at the time of his death, we do know that prolonged vomiting can disrupt the potassium balance in the body.  This disruption could induce cardiac arrhythmias as well as enhance the disruption of the sodium-potassium pump furthering edema in any cell that depends upon this mechanism, including the brain cells.


Mr. Bleecker maintains in Unsettled Matters that prior to the time of his death, Bruce Lee was drinking quite heavily.  Alcohol consumption is one of the factors elicited in SUDEP research, which seems to make SUDEP more likely to occur.  Bruce Lee’s reported alcohol use makes the diagnosis of SUSDEP more likely.


While there have been those who discounted the pathologist’s findings in the lungs at the time of autopsy, these findings may support the diagnosis of SUDEP.  Nashef and Tomson address this issue by saying, “respiratory changes frequently occur in seizures, with well documented central and obstructive apnea, excess bronchial and oral secretions, pulmonary edema and hypoxia.  Pulmonary edema is present in a large majority of SUDEP cases (Nashef & Tomson, 2008).  There was, of course, fluid found in Bruce Lee’s lungs at the time of autopsy.


Compounding the problem is that Bruce Lee was using a machine that enhanced muscle function and was engaged in physical training almost constantly.  Traditional Chinese martial artists have a name for too much training, which is San Gong.  While this certainly is not the cause of death, it may have been factorial due to an increase in lactic acid produced by the muscles from overuse.  This increase in lactic acid could have inhibited the Sodium-Potassum pump, furthering the edema.


Most of the differential diagnosis can be eliminated by examination of the available medical information.  Clearly, Epidural, Subdural, and Subarachnoid hematomas can all be eliminated due to the fact that none of these have been clearly stated as being the cause of his death in any preceding or his death certificate, as well as the pathologist saying “the blood vessels of the brain intact and unblocked.”  There has not been any mention of any pooling of blood found.  A logical conclusion would be that if there was some sort of hematoma found, this would have been pronounced at the time of death, declared as the primary cause of death, and the matter closed at that point.


Many in the martial arts community have presented Dim Mak as the cause of death.  As such, it is being included in the discussion of the differentials.  Dim Mak is the legendary delayed death touch in which the administrator of the Dim Mak delivers the technique to the victim, and the victim dies in variable amount of time.  While there are many accounts of this technique being applied in martial arts history, there is very little acceptance of this phenomenon in Western medicine.


Mr. Bleecker, a well-respected martial artist, biographer, and friend of Mr. Lee, has submitted the question “did Bruce’s life end as a direct result of adrenal crisis associated with brain edema?” and adds “similar to Addion’s disease” (Bleecker, 1996).  It seems highly unlikely that this could be the case, especially after a consultation on May 25, 1973 with “Dr. Harld Karpman who ordered a complete work-up and neurological exam” (Bleecker, 1996).


In this examination, Mr. Bleecker maintains that “Apart from telling Dr. Karpman that he absolutely hated Chinese food, Bruce’s major complaints were that he: (1) had been under a great deal of tension for the past several years, (2) suffered from insomnia, (3) complained of a poor appetite, and (4) had lost twenty pounds over a two-year period.”  Curiously absent from this list of complaints is that he suffered a life-threatening seizure 15 days earlier.


Certainly, a qualified physician would have inquired into what substances Bruce was using; steroid use in any form would have caught the attention of the physician.  Bruce would have been advised to taper off the drugs or to remain on them.


While the author believes Mr. Bleecker presented the most accurate information at his disposal, there have been questions raises as to the validity of Mr. Bleecker’s assertion that Bruce Lee was using steroids prior to his death, resulting in an adrenal crisis or Addison’s Disease.


Although there is some merit to Bleecker’s argument, the facts presented speak against an adrenal crisis or Addison’s disease.  First, there is no representation that there was anything wrong with the adrenal glands at autopsy.  No hypertrophy or atrophy was mentioned.  “Patients with acute adrenal crisis present with high fever weakness, apathy, and confusion” (McPhee, 1995).  Miss Tai Ping did not mention that Bruce Lee had any of the above symptoms, only that he had a headache.  As such, adrenal crisis or Addison’s disease can be ruled out.


Conclusion


Irrespective of any definitive conclusions that are made with respect to the cause of death of Bruce Lee, there will continue to be speculation.  A concise review of the available history and physical information as well as autopsy results demonstrate that he was not a well man exhibiting signs of epilepsy getting progressively worse toward the time of his death.  While the diagnosis of Sudden Unexpected Death in Epilepsy was not well accepted in the medical literature at the time of his death, it was known that people did die from epileptic complications.  It is clear that Mr. Lee had a majority of the factors in his health history that are consistent with a diagnosis of Sudden Unexpected Death in Epilepsy.  As such, it is clear that Mr. Lee died as a result of cerebral edema secondary to complications of epilepsy.  As a result, the death of Mr. Lee should be ruled as a natural death caused by cerebral edema secondary to epilepsy, which is consistent with the phenomena known currently as Sudden Unexpected Death in Epilepsy with the tertiary cause being increased lactic acid brought about by extreme amounts of physical exercise.





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About the Author


Dr. Craig M. Pradarelli, BA, BSc, MD, graduated from medical school the Belize College of Medicine.  He has a Bachelor of Arts in Psychology from Lakeland College, a Bachelor of Science in Medicine and a Certificate in Basic Sciences from the Medical University of the Americas, Nevis, West Indies.  He spent numerous years working as a criminal defense investigator in Milwaukee, Wisconsin working on over 500 homicide cases; he has taught at several colleges in Wisconsin.

His academic interests are in Forensic Medicine, Emergency Medicine and Osteology.  He is a founding member of the Professional Association of Wisconsin Licensed Investigators.





Publisher Dr. Robert O'Block, American College of Forensic Examiners.