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Marler Blog Providing Commentary on Food Poisoning Outbreaks & Litigation

Yes, Stewart Parnell, You Killed Bobby Ray Too With Salmonella Peanuts

Screen Shot 2015-07-01 at 9.18.53 PMStewart, you and your counsel can complain all day that you could have proved the opposite, but that would not have worked.

BOBBY RAY HULLETT’S SALMONELLA ILLNESS AND DEATH

Bobby Ray Hullett, known to friends and family as Pete, and his wife Shirley lived in Maiden, North Carolina. The Hulletts were married for forty-five years and worked together at the Southern Glove mill for thirty years. Pete was a soft-spoken man who worked all his life. Early in his career at Southern Glove a huge press crushed one of his hands leaving him with one functional hand. Despite his hand injury, Pete continued to work uninterrupted at Southern Glove until his retirement shortly before his death.

Pete was also able to take care of the house, garden, and car, which he loved to tinker with. A man of quiet pride, Pete never complained about his misfortune, and taught his sons to never make excuses for themselves. Pete liked football, bowling, and wrestling, but he loved NASCAR. Pete and Shirley were also devoted to their church, which they attended three times a week, and they especially enjoyed the gospel choir. Pete always provided for his family and was Shirley’s constant companion throughout the decades of their marriage.

Shirley Hullett had two young boys from a prior marriage when she married Pete. Pete helped raise the boys, Tony and Dale, and was the only father they knew. When Dale was only seventeen he had a son himself. Dale turned to Shirley and Pete to be surrogate parents. And so Shirley and Pete also raised Dale’s son Bobbie who is now thirty-five and remains devoted to his grandmother. Dale passed away from complications from chronic liver disease in his early 50’s.

At the time of his illness and death, though on high blood pressure and cholesterol medications, Pete was a very healthy person. He was also a frequent consumer of Austin-brand peanut butter crackers. In fact, in the days leading up to the illness that would take his life, Pete ate the crackers as a snack two or three times a day.

Pete’s symptoms began on November 23, 2008, with vomiting and severe dizziness that eventually caused him to lose consciousness and collapse on the kitchen floor. That night, he suffered from excruciating abdominal cramps and experienced multiple bouts of both watery diarrhea and vomiting. The next morning, the severity of Pete’s illness became dramatically apparent. Shirley recalls:

By Sunday night he thought he had a virus, he was up and down all night throwing up and with diarrhea. Monday morning he had gotten up and felt very weak, he took out the trash and came back into the house. He then collapsed on the kitchen floor, and I could not get him up. He asked me to call my son Tony to come help. Tony got off work and immediately came to the house. Tony did not want to wait for the ambulance, so he picked Pete up and put him in the car and drove to the hospital.

In the emergency room at Catawba Valley Medical Center in Hickory, North Carolina, doctors assessed Pete’s condition. After triage in the ER, Bernard Crain, MD, who recorded a blood pressure of 84/56 and pulse of 129, saw Pete. Pete was rehydrated, which brought up his blood pressure slightly, and was given oxygen by mask. Dr. Crain also ordered intravenous Phenergan for Pete’s severe nausea.

Despite being very ill, Pete was able to give a medical history, reporting no heart attack or diabetes, and no prior surgeries or other major health concerns. Dr. Crain ran an EKG that was compared to one done in 2004, and while no significant pathology was suspected, the strip did show sinus tachycardia with a heart rate around 130[1]. Pete had to suffer the placement of a Foley catheter and urine and blood specimens were sent to the lab.

Pete’s lab results were abnormal, indicating decreased kidney function by an elevation in his BUN and creatinine.[2] He was also acidotic, having an increased amount of carbon dioxide in his bloodstream.

Pete was in kidney failure, ill with severe ongoing gastrointestinal symptoms, and had to be admitted to the hospital for further care. Kenton Sanders, MD, saw Pete next, shortly after 5:00 PM on November 24. At this point, Pete was still coherent enough to offer Dr. Sanders a detailed medical history. He related that he had no recent history of antibiotic usage; that he had a vague history of multiple sclerosis for three years; and that he had recently been taking Lipitor, baby aspirin, and another blood pressure medication.

Upon examination, Dr. Sanders thought Pete appeared ill and “quite fatigued.” An abdominal exam revealed tympany to percussion[3], but bowel sounds were present, and there was no tenderness noted. Because of Pete’s severe and ongoing diarrhea, Dr. Sanders’s impression included the comment, “The room has the smell of Clostridium difficile,” and included the diagnosis of acute onset nausea, vomiting and diarrhea suggestive of gastroenteritis. He further indicated that Pete’s kidneys had likely failed as a result of “a prerenal component,” which is a reference to the severe volume depletion and dehydration Pete had experienced as a result of his gastrointestinal losses.

Dr. Sanders admitted Pete to the medical floor on telemetry and pulse oximetry, and he continued his IV fluids and oxygen. He began Pete on the antibiotic Flagyl, and ordered that samples of stool, urine, and blood be tested.

Less than an hour after seeing Dr. Sanders, Pete suffered additional bouts of green, foul-smelling diarrhea. The nurse checked on him periodically to make sure that he was as comfortable as possible under the circumstances. When rechecked around 8:00 PM, the nurse reported that Pete was lethargic, but very alert and oriented, and that he was responding appropriately to questions.

Shortly after 11:00 PM, however, the complexion of Pete’s illness began to change. A portable chest x-ray had been done, which showed no change, and afterward a nurse checking on Pete found him having notable shaking that had not been present just minutes before. His pulse was high—in the 140-150’s—and Pete began talking incoherently. He was also unable to follow the simple command of opening his eyes when prompted. A portable pulse oximetry read 54% on two liters of oxygen, so the nurse increased the oxygen to three liters. There was, however, no change in Pete’s oxygen saturation. The nurse immediately called Dr. Sledge, who ordered that Pete be transferred to the critical care unit (CCU).

In the CCU, Pete was unresponsive when lifted into bed. Shortly thereafter, at just before midnight, the lab called Dr. Sledge to notify him that Pete’s lab values were grossly abnormal and consistent with severe metabolic acidosis.[4]

Just after midnight on November 25, 2008, an electrocardiogram was done that was abnormal, showing sinus tachycardia and signs of an acute myocardial infarction. Dr. Sledge made an addendum note:

I was called by 3rd floor nursing staff due to decreasing level of consciousness and decreasing blood pressure. Patient has been transferred to ICU. ABG reveals severe metabolic acidosis. He was started on bicarb drip earlier tonight by Dr. Sanders due to shallow respiratory and unresponsiveness and will need intubation. I discussed code status with the wife. She wants everything done. Will ask anesthesia to insert ETT and central line.

In the early morning hours of November 25, Thomas Hill, MD, inserted a left subclavian central line and an endotracheal tube (ETT) for mechanical ventilation. Once these were in place, the results of another arterial blood gas study again showed severe metabolic acidosis. A short while later, Pete’s level of consciousness increased, allowing him to better appreciate what was going on. This frightened him badly and, ultimately, wrist restraints had to be used to keep him from pulling out the central line and ETT that Dr. Hill had just inserted. For Shirley, seeing her husband in restraints in the midst of his suffering was profoundly upsetting. Pete seemed to be getting worse by the hour despite the doctors’ efforts.

Physician notes around 2:10 AM indicated that Pete’s urine output was poor, despite receiving two liters of normal saline and ongoing fluid hydration. The differential diagnosis now listed shock, acute renal failure, diarrhea with white blood cells in the stool, and still questioning C. diff, although by history Pete had not been on any recent antibiotic therapy[5]. Respiratory failure was also now listed in the differential along with metabolic acidosis. Laboratory results at 2:43 AM showed liver dysfunction and continued kidney dysfunction.

At 4:00 AM on November 25, 2008, Pete was awake and looking at the nurse, squeezing her hands, and moving his toes on request. However, at 5:00 AM, blood gas alarm values were reported by the lab, again with significant metabolic acidosis, as reported to Dr. Sledge.

Pete’s family was in the room with him at 7:00 AM when the ICU/CCU physician came in to see him. He explained to them that Pete had suffered an acute myocardial infarction (MI) with cardiogenic shock and that his prognosis was poor. He was producing very little urine and was in acute renal failure. He remained on the ventilator, and the doctor indicated in his chart notes that Pete might not survive the day.

For Shirley, Pete’s hospitalization was a long nightmare. She never spoke to him again after Tony took him to the hospital because he was on a ventilator; she could only watch his torment as his life ebbed away. Her memories are vivid:

He had needles stuck in him, it seemed like there were fifteen to twenty needles total. I told him I loved him, I asked him if he loved me and with a pitiful look he nodded his head yes. It broke my heart to see him in this condition; the doctor told my family and myself that there was not a doctor in the United States that could save him. Every organ in his frail body was shutting down,

At 9:00 AM on November 25, Pete was awake but lethargic. The doctors gave him vasopressors to keep his blood pressure up. He still wore the wrist restraints so he would not pull out his breathing tube. The doctor came in to discuss Pete’s condition with the family again. Tony recalls that while Pete was unable to talk, his eyes reflected the pain of his overwhelming infection.

At about 9:30 AM, Sanjay Patel, MD did a cardiology consultation. Dr. Patel reviewed the history that had brought Pete to the ER and his subsequent admission event. He noted no prior cardiac history but that Pete had reported hypertension and hyperlipidemia. Pete’s cardiac labs were consistent with a recent infarct. Dr. Patel’s impression was shock with a possible cardiogenic component, but with his concurrent renal failure thought the cardiac component to be less likely. He agreed that Pete’s prognosis was not good.

At about 11:00 AM the same day, the laboratory called an alarm value to Dr. Kaariainen, which was to report that the blood cultures drawn the day before were showing positive growth of gram-negative rods. At about 12:25 PM, an IV with the antibiotic Levaquin was started. At 4:00 PM, Pete accidentally pulled out his arterial line, and respiratory therapy came in to try to place a new one without success.

At 10:00 PM that night, Pete was still alert enough to move his arms and feet a little when asked, but his hands were cold and cyanotic to exam. Serology for C. diff was negative. A stool sample was positive for occult blood, but negative for the protozoan parasites Giardia and for Cryptosporidia.

At midnight on November 26, 2008, Pete was still alert and oriented, but lethargic. But by 4:00 AM on the 26th Pete’s level of consciousness was declining. His eyes were partially open, but there was no response to verbal stimulation. The doctor discussed Pete’s grave and worsening condition with Shirley. Pete was no longer responding, although his eyes were open and he appeared to look around. His laboratory results reflected progressive organ failure.

At 8:00 AM nurse notes indicate that Pete was obtunded but did arouse to pain. Dr. Luney came in to evaluate him and reviewed his chart and labs, and confirmed his prognosis was grave. He continued to diagnose shock, hypotension, acidosis, and multiple organ system failure, now with lab evidence of liver failure as well as renal failure.

At 11:30 AM on November 26, hospice came in to consult with the family and to discuss the procedures they should follow when Pete experienced cardiac arrest, which they fully expected. They decided on a partial code procedure, as they were still awaiting other family members to arrive and did not want to terminate life support until later in the week.

Pete continued to decline throughout the day on November 26. His heart rhythm worsened and though his blood pressure held at greater than 100 systolic, he remained unresponsive and his skin continued to show mottling. At 6:20 PM, Pete’s blood pressure suddenly fell, and drugs to support blood pressure were given, but had no effect. Pete’s family was summoned. As Shirley and Bobby entered Pete’s room, Pete rose up slightly from his bed to look at them, fell back, and was gone.

With his family at his bedside, Bobby “Pete” Hullett was pronounced dead at 6:32 PM on November 26, 2008, the day before Thanksgiving.

Two days later, Pete’s blood cultures were finalized as positive for Salmonella group. In his “Death Summary,” of November 26, Dr. Kaariainen included the following diagnoses at death:

  1. Multifactorial shock including cardiogenic shock, septic shock and hypovolemic shock
  2. Respiratory failure with ventilator support and significant difficulty Inadequate oxygenation despite 100% FI02 saturation settings on the ventilator
  3. Large acute myocardial infarction, troponin peaking at 45
  4. Acute liver failure from shocked liver
  5. Severe oligo-anuric acute renal failure from acute tubular necrosis from shock
  6. Severe underlying metabolic acidosis including lactic acidosis, suspected likely ischemic colitis
  7. Ongoing upper gastrointestinal bleeding with anemia
  8. Hyperkalemia
  9. Leukocytosis
  10. Multiple other medical comorbidities contributing as noted In the admission history and physical

Dr. Kaariainen commented, “He was felt to be in shock from a multifactorial etiology including cardiogenic shock from his acute MI, hypovolemic shock from diarrhea and dehydration, as well as probable sepsis from an intra-abdominal source given his severe unresponsive metabolic acidosis and lactic acidosis.”

The “Death Summary” also explained that Hickory Cardiology Associates was consulted and that Pete was treated medically for his acute MI with the limitation that “we were unable to use significant doses of ACE inhibitors or beta blockers given his already pre-existing acute renal failure and hyperkalemia as well as his profound hypotension.”

On December 23, 2008, Pete’s stool culture that had been collected on November 25, 2008 was issued the final result: positive result: SALMONELLA TYPHIMURIUM – HEAVY GROWTH.

CAUSATION

It is clear that Mr. Hullett’s Salmonella infection and death are directly linked to his consumption of contaminated Austin-brand peanut butter crackers manufactured by Kellogg Company.

Specifically, Mr. Hullett consumed Austin-brand peanut butter crackers on a near-daily basis in the days leading up to the onset of his illness in November 2008. The crackers were purchased as a local Food Lion grocery. He began to suffer from symptoms consistent with a Salmonella infection around November 23, 2008, and a stool sample submitted on November 25, 2008 confirmed his Salmonella infection. Also, a blood sample collected on November 24, 2011 cultured positive growth of gram-negative rods, confirming that bacteria were in his blood stream.

Further testing revealed that he had been infected with Salmonella serotype Typhimurium. Pulsed Field Gel Electrophoresis (PFGE) fingerprinting of the bacterial isolate revealed a genetic match to the pattern linked to the nationwide outbreak strain of Salmonella associated with contaminated PCA peanut product used by Kellogg Company in the manufacture of its peanut butter crackers.

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[1]           There were also frequent premature ventricular contractions, but the doctors felt that was unchanged from Bobby’s prior EKG.

[2]           Creatinine is a breakdown product of creatine, which is an important part of muscle. A serum creatinine test measures the amount of creatinine in the blood. The normal range (NR) for creatinine is <1.2. A high level of serum creatinine is a marker of poor kidney function, because its presence at high levels shows that the kidney is not functioning properly to eliminate this by-product from the blood. The other such marker used is blood urea nitrogen, or BUN, which forms when proteins are broken down. The normal range for BUN is 5-17.

[3]           Tympany on a physical exam is a resonating sound typically due to intestines distending with gas.

[4]           Metabolic acidosis often occurs in the setting of acute renal failure as the kidneys normally remove acid from the body.

[5]           Clostridium difficile bacterial infections often occur in patients who have recently taken antibiotics with the resulting disruption of their normal intestinal flora which creates an opportunity for C. diff. to overgrow resident bacteria and cause diarrhea. Pete would test negative for C. diff.