C ANADA

Province of Alberta

Report to the Minister of Justice and Attorney General Public Fatality Inquiry

Fatality Inquiries Act

WHEREAS a Public Inquiry was held at the in the on the on the before into the death of of

Calgary Courts Centre Calgary

, in the Province of Alberta, , ,

City
(City, Town or Village)

of day of day of

(Name of City, Town, Village)

16th 19th
November 8 & 9, 2012

January January

2011 , (and by adjournment

year

2011 ),Feb, 8/11, May 16/11 &

year

John D. Bascom
Ashish Toews
(Name in Full)

, a Provincial Court Judge, 33 yrs

(Age)

121 Harvest Creek Crescent NE, Calgary, Alberta

(Residence)

and the following findings were made:

Date and Time of Death: Place: Medical Cause of Death:

July 31, 2008 at approximately 13:50 hours Foothills Medical Centre, Calgary, Alberta

(cause of death means the medical cause of death according to the International Statistical Classification of Diseases, Injuries and Causes of Death as last revised by the International Conference assembled for that purpose and published by the World Health Organization The Fatality Inquiries Act, Section 1(d)).

Presumed fat embolism. (Refer to page 3 for medical cause of death).

Manner of Death:
(manner of death means the mode or method of death whether natural, homicidal, suicidal, accidental, unclassifiable or undeterminable The Fatality Inquiries Act, Section 1(h)).

Unclassified. (Refer to page 7 for continuation of Manner of Death).

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Circumstances under which Death occurred:

1) Mrs. Ashish Toews, a healthy 33 year old female had abdominoplasty with liposuction on July 18, 2008 at a private plastic surgery clinic in the City of Calgary. After surgery she experienced some respiratory problems which had resolved themselves at the time of discharge. The following day she experienced nausea, vomiting, headaches and pain around the surgical area. The headaches worsened and she was transported by ambulance to the Foothills Medical Centre. Her condition worsened and she died on July 31, 2008.
Recommendations for the prevention of similar deaths:

2) It appears Mrs. Toews died as a result of fat embolism syndrome causing a cerebral edema which resulted in death. It is clear from a review of all medical testimony that fat embolism syndrome is extremely rare in situations such as that of Mrs. Toews. It is possible that there were other factors which lead to her death. It might be said, as stated by Dr. Merchant, that Mrs. Toews should have been transferred from the surgical centre to a hospital. However, there is nothing to suggest with certainty that this would have prevented her death. It is not possible for this court to make recommendations based on the evidence heard.

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Medical Cause of Death: 3) On July 18, 2008 Mrs. Ashish Toews underwent an elective procedure at a private surgical clinic. Subsequent to the surgery she developed medical complications and was hospitalized on July 18, 2008. Dr. Michael Dunham, a specialist in critical care diagnosed Mrs. Toews as suffering from fat embolism syndrome. Her condition worsened and she died on July 31, 2008. 4) Dr. Sam Andrews, Deputy Medical Examiner and pathologist, performed the autopsy on Mrs. Toews. Dr. Andrews reports are Exhibit 1, tabs 4 and 5. At tab 4, Dr. Andrews summarized his findings: According to reports, the decedent was admitted to the Foothills Medical Centre on July 19, 2008 with trouble breathing (dyspnea) and a severe headache. She was awaiting admission in the emergency department when she had a seizure. A computed tomography (CT) scan showed brain swelling (cerebral edema) and increased pressure within the head (intracranial pressure). Her condition deteriorated and she died. Apparently she underwent a tummy tuck (abdominoplasty with liposuction) at a private plastic surgery clinic on July 18, 2008. She was told she was discharged with water on the lungs. Fat embolism syndrome is a difficult clinical diagnosis and is rare but serious complication of liposuction. It is thought that during the liposuction procedure, fat globules are introduced into veins in the area that subsequently travel to the lungs, brain and other organs (fat emboli). The three classic symptoms of fat embolism syndrome, respiratory distress, cerebral dysfunction (delirium, lethargy, confusion and seizures), and a petechial (pinpoint hemorrhages) rash, usually appear within 12 - 72 hours after the procedure. Cerebral edema (swelling of the brain) may contribute to the neurological dysfunction. In this case, the cerebral edema was severe resulting in obstruction of blood flow to the brain resulting in death of portions of the brain (infarction). Unfortunately, there were no autopsy findings of fat embolism syndrome in this case. The salient gross findings are pinpoint hemorrhages of the skin and conjunctivae (eyes), pinpoint hemorrhages of the brain (white matter). Microscopically, fat emboli and readily demonstrated in specially treated and stained tissue. However, there is no literature describing delayed death due to fat embolism syndrome and the presence or absence of microscopic fat emboli. Since the clinical findings were very suggestive of fat embolism syndrome and the autopsy demonstrated no other reason for the decedents death, the cause of death was certified as presumed fat embolism syndrome.

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5) Dr. Zygun, a specialist in critical care, took over the primary care of Mrs. Toews on July 25, 2008. He also confirmed a diagnosis of fat embolism. He testified that such diagnosis was difficult, in that there was no definitive test. His diagnosis was based on a constellation of symptoms. (January 20, 2011, transcript page 131). 6) Dr. Richard Merchant, a specialist in anesthesiology, testified via closed circuit TV from Vancouver. Dr. Merchant spoke of laryngospasm and negative pressure pulmonary edema, a diagnosis recorded by Dr. Nanji, Mrs. Toews anaesthesiologist. Dr. Merchant concluded the following from Exhibit 9: The sequela of negative pressure pulmonary edema is not well addressed in the medical literature. Most reports are single cases or small series from single institutions and report generally complete recovery within generally 24 hours, though severe cases requiring airway support, intubation, and intensive care unit management are described and clearly take longer to resolve. Pathological examinations and the course of pathologic changes are not information that I have been able to find. In discussion with ICU and pulmonary medicine colleagues I have been told that pulmonary edema of this type, due to pressure changes between pulmonary capillaries and air spaces, are not felt to be associated with pathologic changes in the lung structure, and thus, that once recovered, the lung is recovered and not susceptible to or at risk of further damage. You have asked the following specific questions: 1. What effect, if any, the laryngospasm and negative pressure pulmonary edema had on her cause of death as determined by the Medical Examiner, i.e. presumed fat embolism syndrome. These two pathological conditions are distinct entities and on the face are not related. I can find no literature describing such an association: I see the question in several parts: Could the high negative intrathoracic pressures generated during the laryngospasm have caused the fat embolism (in essence, sucked the fat into the bloodstream from the disrupted tissues)? I am aware of no evidence that such an etiology exists. Could the pulmonary edema, and any associated lung changes, have allowed circulating fat globules greater access to the systemic circulation (and the brain) and thus worsening the potential fat embolism syndrome promoted the further deterioration? Again I am not aware, nor can I find in my review of the academic literature, any suggestion that such a pathological course can be produced; further, it seems likely that the cerebral effects of fat embolism are not specifically related to circulating fat globules but rather to the development

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of metabolic or biochemical processes associated with trauma to fatty tissues. While the pathological mechanisms of the two complications are distinct, both are expressed in similar fashions: i.e. both are associated at a cellular level with hypoxia in the brain. Could the hypoxia caused by the negative pressure pulmonary edema be associated with a more severe expression of the subsequent CNS effects of the presumed cerebral fat embolism syndrome? By extension, would more aggressive treatment of the NPPE have perhaps diminished the severity of the injury produced by the fat embolism syndrome? While this does not seem to me to be likely, I cannot find a specific answer to this question, and I think it needs to be directed to a referee more familiar with the pathophysiology of this type of acute brain injury.

2.

Whether the laryngospasm and the negative pressure pulmonary edema was the cause of the patients death (instead of the presumed fat embolism syndrome...) That does not seem realistic to me. Insofar as I am aware, the NPPE syndrome is entirely a pulmonary event, and the patient appeared to have largely recovered the day following the operation. The ambulance attendants record that there were no pulmonary complaints: Chest: no complaints. No chest pain/discomfort. No respiratory distress, and her oxygen saturation was recorded at 97% twice. The initial deterioration in hospital: a rapid onset of decreased level of consciousness and a seizure are not recorded to be associated with any respiratory complaint, or potential hypoxia. The complaint of severe headache with the seizure, cerebral edema and sequelae seem to indicate the cerebral complication as the index event culminating in death.

7) Dr. Juan Ronco, a specialist in critical care medicine, testified via CCTV from Vancouver. In his report, Exhibit 6, he states the following: During the decades of 1980s and 1990s, a number of reports described the phenomenon of postoperative hyponatremia resulting in death or permanent brain damage (8,9). The reported cases occurred mainly in previously healthy individuals following elective surgeries, and most of the patients who died or suffered permanent brain damage were women of reproductive age (menstruating women). These patients typically presented with a prodrome of headache, nausea, vomiting, and weakness. Progressive deterioration in these reported cases led to obtundation, grand mal seizures, respiratory arrest and or pulmonary edema likely as a result of hyponatremic encephalopathy and ensuing cerebral edema and intracranial hypertension.
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In post-surgical patients, there is a known state of increased secretion and levels of ADH secondary to pain, nausea and or intravascular volume depletion, with the ensuing retention of water out of proportion to sodium (a phenomenon otherwise called desalination) (9). Whereas most elder adult patients with symptomatic hyponatremia and sodium levels less than 128 mmol/L do not suffer brain damage, there is an increased susceptibility in younger women of reproductive and menstruating age to suffer brain damage from postoperative hyponatremia. A review of the reported cases of younger women suffering brain damage as a result of postoperative hyponatremia revealed sodium concentrations ranging from 104 to 130 mmol/L with a mean of 117 mmol/L (10). Susceptibility of young menstruating women to hyponatremic encephalopathy and brain edema appears related to estrogen levels interfering with the mechanisms of adaptation of neurons to hypotonicity (extrusion of intracellular sodium via Na-K ATPase activity is inhibited by estrogens) (11). In addition, hypoxemia is a major factor contributing to brain damage in patients with hyponatremia (11-13). Hypoxia interferes with brain ion transport, which allows the brain to adapt to increases in cell water. The adaptive increase of Na-K-ATPase transport activity, which is initiated by hyonatremia, is severely blunted by hypoxia, thus causing a net increase in brain sodium and resulting in brain edema. Among patients with hyponatremic encephalopathy, the progression to death or brain damage is frequently associated with hypoxemia. Hypoxia is also a major stimulus for increased secretion of ADH. Elevated plasma ADH levels in hyponatremic patients increase water movement into the brain and thus worsen brain edema. In patients with sumptomatic hyponatremia, respiratory arrest often occurs very abruptly (14). The occurrence of a hypoxic event such as respiratory insufficiency is a major factor militating against survival and or permanent brain damage in patients with hyponatremia. The combination of systemic hypoxemia is far more deleterious than is either factor alone. The finding of serum sodium of 129 mmol/L associated with the constellation of symptoms Mrs. Toews experienced while at home and en route to hospital are, at least, very suggestive of a hyponatremic encephalopathy. Whether her symptoms while at home were the result of FES, hyponatremic encephalopathy and or a combination of both is difficult to discern. From the pathophysiological stand point, it is theoretically possible that the perioperative hypoxemia she experienced might have contributed to the increased secretion of ADH with the ensuing aggravation of her water homeostasis and hyponatremic encephalopathy and other causes of cerebral edema. Fat embolism syndrome is a rare but well reported complication of liposuction (15, 16, 17). Albeit reported rarely in case report form, it is likely that, given the variable presentation of FES, its incidence following liposuction is underestimated in the literature.
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Interestingly, Fourme and coworkers reported in 1998 a case similar to the present one (2). After receiving a similar general anesthesia and intravenous fluids, a 29 year old healthy woman experienced acute hypoxemic respiratory failure within one hour of completion of a liposuction of 600 ml of fat (reference). The diagnosis was confirmed after analyzing specimens obtained via bronchoscopy and the patient recovered clinically and radiographically within two days, and was discharged from hospital at the third day of hospitalization. Up to 1998, only 6 cases of liposuction induced FES have been reported and only one presented with neurological manifestations after surgery (15, 16). It is possible that fat embolism was responsible for this woman course not only in the ICU but also during the anesthesia recovery and postoperative period. Certainly, although the timing of the presentation is earlier than most reported cases of fat embolism, the predisposing surgery, the clinical constellation and the indirect evidence presented in the post-mortem examination make FES a likely explanation for the events. Whether this occurred in isolation or concomitantly to negative pressure pulmonary edema and or hyponatremic encephalopathy is difficult to discern. It is possible that the combination of hypoxemia and cerebral edema led to refractory intracranial hypertension and that both processes therefore contributed to the fatal outcome. 8) The review of the evidence leads me to conclude that the cause of death was a cerebral edema caused by fat embolism syndrome. As indicated by Dr. Ronco there may have been other factors which lead to the cerebral edema. It cannot be determined whether fat embolism syndrome occurred in isolation or concomitantly with other factors.

Manner of Death Contd: Unclassified. 9) Mrs. Ashish Toews, after having an elective procedure at a private plastic surgery clinic in the City of Calgary, experienced a tonic/chronic seizure and did not regain consciousness. A CT scan of the head showed that Mrs. Toews had suffered a generalized cerebral edema as well as a possible pulmonary edema. Her condition worsened and she died on July 31, 2008.

Dated: April 19, 2013 at Calgary, Alberta John D. Bascom A Judge of the Provincial Court of Alberta
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