Please click on the titles below to go to the corresponding sample Case Evaluation Reports.
Bronchoscopy For Diagnostic Purpose Under General Anesthesia, Mismanaged Resulting in Death in the Recovery Room.
At age 69, this patient with chronic psychiatric problems, was hospitalized on 8/1. Because of a recent cough and breathing problems not responsive to antibiotics, and a chest x-ray consistent with widespread pneumonia or broncho-alveolar carcinoma, she was seen by a Pulmonary Specialist who correctly recommended a fiberoptic (thin, flexible fiberoptic telescopic device) bronchoscopy examination of the inside of the passageways (trachea, major and minor bronchial tubes) of her lungs as well as sampling the lung secretions for germs and cancer cells, as well as a brush biopsy (like a Pap smear), and a trans-bronchial biopsy (piercing a bronchial tube to sample the deep lung substance),
Because of her severe anxiety and panic attacks, it was reasonable to suggest that this procedure be performed under general anesthesia. Before the anesthesia, arterial blood gas studies revealed impaired oxygen saturation in her blood (80-90%) even with nasal oxygen supplementation. On call she also received a tranquilizer tablet.
She was placed under general endotracheal anesthesia from 10:30 a.m. until 11:20. The CRNA (Certified Registered Nurse Anesthetist) was Kevin and the Anesthesiologist is Dr. Larry (was this doctor there all the time, and in the recovery room too?)
Dr. David performed the fiberoptic bronchoscopy and saw no lesions in her bronchial tubes. He also performed the bronchial lavage (washing), the brush biopsies, and the trans-bronchial biopsy. He had no difficulties, and his procedure was done through the endotracheal tube in a breathing but anesthetized patient. Generally there are only two safe times to remove the endotracheal tube: when the patient is breathing well but still asleep (still under anesthesia), or fully awake and demanding the endotracheal tube be removed. But in her case, because of her severe lung disease noted on her chest x-ray and by the impaired oxygen transport ability into her blood, the only safe time would be when she was fully awake. Not doing this is a departure from the accepted standards of care in my opinion. It put her in a zone of danger. This is the responsibility of the M.D. Anesthesiologist, the CRNA, their corporation, Dr. David (since he obviously was fully aware of the severity of her pulmonary condition), his Corporation and the Hospital.
According to the anesthesia record: “Breathing spontaneously, extubated (endotracheal tube removed), to PACU (Post Anesthesia Care Unit: Recovery room) with oxygen mask. According to the dictated operative report by Dr. David (dictated at 12:30 a.m. on 8/9): “After the patient was extubated in the recovery room, the patient had increased respiratory difficulties and ultimately had to be reintubated.” He had a duty to stay with his patient, especially if the M.D. Anesthesiologist was not present; this would put the “other M.D.” in charge and to some degree, in charge of the CRNA, even if he was a Surgeon, and especially as a Pulmonary Disease Expert.
Dr. David was present, according to the note on the Anesthesia Record, when she was reintubated with a 7.0-mm size tube.
According to the PACU page, she arrived there at 11:45, and from “0 to 2” had a “1” for “Respiration,” a “0” for “Consciousness” and a “1” for Oxygen Saturation. This was inadequate. At 11:45 the nurses notes (which are difficult to read) state respiratory problems and “jaw support attempt but not sufficient.” Pulling up on the jaw helps to pull the tongue away from the upper windpipe. Dr. Nick (apparently an Anesthesiologist) was present. But she was intubated by CRNA #1? Why was the less skilled person allowed to do this more difficult intubation, especially when Anesthesiologists should be available: they have the needed greater skill? The failure to have the most skilled person attempt to intubate is a departure from the standards of care.
That Nurse’s note says “Bilateral (both sided) breath sounds.” But was it from her spontaneous respiration sounds they (who listened???) heard or was it really from the endotracheal tube securely positioned in her windpipe??? How far was it inserted? Did they use the hand ventilator (“bag”) to force air into her lungs and listen at the same time to be sure that it was in the trachea (after they inflated the balloon that surrounds the lower inch and seals the space between the endotracheal tube and the trachea)?
That Nurse’s note says that the heart rate (H.R.) decreased to 40 at 11:50. Instead of the obvious low oxygen (and did she have a continuous transcutaneous [skin] monitor on as she should have because of her much higher risk factors??); instead of confirming the proper secure position of that endotracheal tube, they gave her the drug atropine to attempt to chemically speed up her heart rate. Who ordered it and why? It had no effect per that note. So at 11:53 she was given epinephrine (adrenaline) “per ordered,” by whom? This, instead of rechecking on the patency and control of her airway, jumping to chemicals instead of confirming her airway, is negligent. This is negligence of the CRNA, the Anesthesiologist(s), Dr. Nick and Dr. David.
Dr. David ordered Lasix (a potent diuretic) instead of confirming the airway. Then she “arrested.”
The “Code Blue” (arrest) sheet said “ventilations started at 11:45 bag valve device” and that she was “intubated, time 11:47, by CRNA Kevin.” It said personnel responding: Dr. David, Dr. Harold, Dr. Paul, Dr. Nick (what time did each get there), as well as: Ann, R.N., Karen, R.N., Earnie, R.T. (Respiratory Therapist), Kevin, CRNA and Dr. Marie (? signature) signed it. Depose them.
After a chest x-ray was done at 12:05, a chest tube was placed between her ribs into the pleural space (between the lung and the rib space) to rule out air pressure squeezing her lung as a cause of the problem (tension pneumothorax) which was not found. It notes, “per M.D. ETT (endotracheal tube) repositioned.”
The Anesthesia / PACU note by what appears to be Dr. Nick says she was “in obvious respiratory failure – PO2 (oxygen blood pressure) 70s (very low), poor respiratory movement/supraclavicular retractions (as she tried to inhale, her flesh sucked into toward her lungs because of airway obstruction, not just inability to breathe because of “poor” effort), being assisted by CRNA.” If that is the case, they all are grossly negligent because if the tube was correctly positioned and she was “assisted,” there should and could not be retractions. If no tube was in place, watching her struggle with her severe lung disease and delaying inserting the tube is also negligent.
It is obvious that the balloon cuff was obstructing her airway that tube must be securely taped to prevent any slippage. Its length must be looked at to be sure enough is inside her windpipe, and that it did not move. The note goes on to say: “Very little air exchange on auscultation (finally “they” listened to her chest), determined reintubation necessary, 7.0 ET (endrotracheal tube) placed by o.k. and breath sounds but severe rhonchi (coarse breath sounds) on left. Discussed with Dr. David – suspect tension pneumothorax…” (he put in the chest tube). “CPR initiated during this time. After this, ventilations not appreciably improved. Abdominal distention noted (because the tube was put into her esophagus [food pipe] which is behind and parallel to the trachea and pumped her stomach full of air). Repeat laryngoscopy (looking into the back of her throat with a lighted instrument) by Kevin, CRNA reports tip of ETT is in the glottis (vocal cord space) with cuff herniated (slid up too high and not fully in trachea and can block the airway) reintubated (by whom?) with confirmation of improved breath sounds bilaterally now.”
He also passed a stomach suction tube down her esophagus to decompress her stomach which as distended pushes up on her diaphragm (breathing muscle) and further compress her lungs like a piston pushing up from below. “CXR (chest x-ray) taken during CPR showed ETT in esophagus prior to being repositioned” (that report is missing. Obtain it and good copies of all the x-rays). “Am concerned that patient suffered a period of anoxia (lack of oxygen) from combination of inability to ventilate prior to thoracostomy (chest tube insertion) with unknown period of ETT not adequately ventilating trachea. Suspect ETT became dislodged during chest compressions at about the same time that thoracostomy was performed.” Who was the doctor in charge?
However, the Nurse’s notes clearly show that she was reintubated the second time (the first intubation was prior to the bronchoscopy and then removed), before she arrested, and it was not timely and/or properly done or she would not have arrested from anoxia. The ETT was “repositioned” at 12:05. She was “reintubated” at 11:47 and “repositioned” at 12:05.
Before she was reintubated at 11:47, too much time elapsed from their negligence’s and the first “vital signs” on the Code Blue sheet start at 11:58 with a heart rate of 30 and no respirations (she was “assisted” by the “ambu” – hand bag). It takes a few minutes of anoxia to cause the heart to slow and then went to “0” at 12:01.
All of this was preventable by not removing the ETT in the Operating Room, properly monitoring her breathing and blood oxygen levels, by timely and correctly reintubating her and securing the position of ETT.
There was no other cause of her severe brain damage. She had good care afterward including tests which confirmed that the only cause of her brain damage was from anoxia. She died on 8/19.
I cannot find the lung biopsy pathology report. The Physician’s “progress note” claims it shows cancer: Broncho-alveolar carcinoma. I did see the report from the bronchial washings that showed “clusters of cytologically malignant cells, consistent with origin of adenocarcinoma.” The brush biopsy was inconclusive. And based on the diffuse findings on the chest x-rays, she most likely had broncho-alveolar carcinoma which is a less common form of lung cancer. It also is the most virulent and does not respond to chemotherapy or radiation therapy, in my opinion. It cannot be removed by surgery since it involved both lungs.
I believe her longevity would have been weeks to a few months based on the extent of the x-ray report changes and her impaired oxygenation. She would have died as a lung cripple and with severe emotional distress based on her psychiatric history of severe depression and fears of death.
That was the ironic effect of their negligence: It eliminated what would have been an extremely traumatic slow death she would have experienced, day by day. There was no excuse for all their negligence, but the Defense will obviously raise these issues.
I would recommend that you authorize that the Medical Review Foundation, Inc. has all these records (and the missing documents) reviewed by Board Certified Medical Experts in Anesthesiology, Oncology (Cancer Therapy) and Pulmonary Disease.
We look forward to continue assisting you with this interesting and important case.
Back to Top
Sedative And Narcotic Overdose During Anesthesia Causes Cardio-Respiratory Arrest And Permanent Brain Damage.
This 30-year-old lady, weighing 130 pounds and 5 foot 2 inches tall wanted plastic surgery to remove abdominal and back fat, as well as fat injections in the buttock are to help elevate it. She had liposuction and fat injections by Dr. “O” in his clinic under local sedation analgesia given by Dr. “M” and Registered Nurse Anesthetist “A” on 01-15-2006.
After signing the surgery and anesthesia consent forms she was given 10 milligrams of Valium by mouth at 8:30 AM. This made her drowsy by the beginning of the anesthesia at 10 AM. At 9:45 AM she received an injection of 4 milligrams of Zofram which helps prevent nausea and vomiting caused by narcotics such as Fentanyl she would be receiving during the procedure for pain control. She also received the antibiotic Ancef at 9:50 AM. All this is reasonable.
Surgery began at 10:30 AM. It abruptly stopped at 1:20 PM because of her unrecognized respiratory arrest that was the proximal cause of her reversible cardiac arrest which was treated by cardio-pulmonary resuscitation. Dr. O inserted an endotracheal tube into her windpipe for good ventilation control while the cardiac compressions and medication was given to help stimulate her heart.
An unknown Cardiologist also was immediately summoned. He interpreted the two EKGs as showing “sinus tachycardia” (rapid heartbeat, most likely as a response to her injection of atropine and epinephrine. The narcotic reversal medication Narcan was also given to overcome any lingering respiratory depressant effect of the narcotic Fentanyl, and he said: “Narcan was administered without any change in mental status”, because her brain had been irreversibly damaged form being without adequate oxygen for too many minutes.
After three to five minutes without adequate oxygen the brain cells (neurons) will die. This is called anoxic encephalopathy, and that was her final correct diagnosis at the Medical Center. Their two CT scans also showed no evidence of any stroke (intra-cerebral hemorrhage or blood clot blocking oxygen rich arterial blood to her brain causing localized areas of gangrene).
Dr. O stated in his 1/25/2006 3:00 PM note: “After almost two hours into procedure, patient helped herself to turn over for second part of surgery and was again seated for back liposuction and fat injection to buttocks.” He further stated: “All vital signs (blood pressure, pulse and respirations) were stable throughout first 3 hours of operating room time, including more than 1 hour of prone position, until about 1:18 PM when a rather sudden drop in heart rate, saturation of oxygen in her blood, and blood pressure was observed. Patient was rolled over to the supine position and case was aborted.”
He also wrote: “In view that there was no improvement in vital signs after initial tip (what does he mean? Does he mean turning supine: onto her back?), we proceeded with OTI (oro-tracheal intubation) and immediately starting CPR (cardio-pulmonary resuscitation and ACLS (standard cardiology life support procedures). All care AFTER they begun the ACLS protocol, and all subsequent care in the two hospitals was very good, but because of the severe lack of oxygen for too long a period of time the care of Dr. O and his Nurse Anesthetist, she sustained irreversible brain damage.
Her cardiac instability after this arrest was caused by that arrest, and was managed properly.
At the Medical Center on CT scan noted a “possible” small pulmonary embolism (blood clot) in one of the branches of a pulmonary artery to her lung. The pulmonary arteries receive venous blood which is saturated with oxygen in her lungs. She had no evidence for any source of any such possible embolism: she had no leg swelling and was not high risk since she was not taking birth control pills, had no previous history of thrombophlebitis (leg vein clots) or pulmonary embolism, and this would be highly unlikely after only a few hours immobile lying on an operating room table. In fact, her treating Physicians concluded that even if it was a pulmonary embolism, it was way too small to be clinically significant: could not have caused her arrest.
The other initial issue raised but never seriously considered was of fat embolism caused by the injections of fat, with some entering her circulating blood. First of all, the standard for injections is to first pull back on the handle of the syringe to be sure that its tip was not inside a blood vessel, so if that was the cause of her arrest, it would be from negligent technique. But with fat embolism of any significance to cause a medical problem, there would be serious blood changes that usually would cause bleeding, and none were present. It was initially raised on the differential diagnosis laundry list but never considered thereafter.
Through discovery you need to determine exactly when Dr. O was in the operating room and during that time(s), exactly what he was doing and what he delegated to the Nurse Anesthetist under his control and for whom he is also directly responsible, as is the clinic who employed them for her “sedation analgesia” care, as well as each of their professional corporations, if any.
If either had a history of previous negligence, then the Surgeon would also be liable. But since he was looking directly at her skin and any bleeding areas, he also had an opportunity to see any cyanosis (bluish discoloration from decreasing and lack of oxygen). Some would consider him to be “the captain of the ship”, but that is a legal question you can answer.
Tranquilizing and sedating drugs such as Valium, the 10 milligram (high) dose she received prior to surgery and which made her sleepy but easily arousable, plus the intravenous Versed have strong warnings concerning their respiratory depressant effect.
They inhibit the body from breathing and can cause a respiratory arrest (which initially causes a slow heartbeat: bradycardia, as noted by the Surgeon in his hand written operative report and then the hypotension (low blood pressure, shock) he also noted that followed the hypotension).
That is classic for unrecognized and not timely treated hypoxia (low blood oxygen that also affects the heart, but this organ is much more tolerant of low arterial oxygen than the brain, which is the reason why her heart was able to be resuscitated, but not her entire brain).
Fenatnyl is a very potent narcotic that was used to help control her pain during the surgery. By itself, high doses are notorious for causing respiratory depression and this drug also comes with the strongest warnings.
The combination of sedatives (Valium and Versed) in combination with narcotic medication (Fentanyl) both come with the strongest warnings required by the FDA and these drug manufacturers as noted in their drug inserts (as also reprinted in the PDR: Physicians Desk Reference) and absolutely very well known by all Doctors including Anesthesiologists and their Nurse Anesthetists.
In this case she initially has a 2 milligrams intravenous injections of Versed at 10:00 AM plus 50 micrograms of Fentanyl. Another similar doses of both at 10:30, followed by 1 milligrams of Versed and 25 micrograms of Fentanyl each five more times until 12:30. The anesthesia fails to show when she was turned prone. That is negligent record keeping, but the Anesthesiologist’s note claimed it was “after almost two hours”, but was that after the start of analgesia at 10:00 AM or when surgery began at 10:30 AM?
The drug manufacturers and the FDA warns to use 30 percent less Versed when patients have received pre-medication, which in her case was the 10 milligrams of Valium. Furthermore, they warn that the maximum dose should not exceed 5 milligrams. She received 9 milligrams.
In addition they warn the loading (initial higher) dose of Versed should be .01 to .05 milligrams per kilogram (0.5 to 4 milligrams) for a “typical adult”. She weighed 130 pounds which is 59 kilograms, so her maximum loading dose would be 2.95 milligrams, but the lowest dose with opioids (narcotics), which would clearly include Fentanyl. Therefore 2.9 milligrams plus 1 milligram per hour thereafter comes to 2.9 plus 3 = 5.9 milligrams, NOT 9 milligrams.
Her total dose of Fentanyl was 225 milligrams during that same time period.
That is excessive, considering her pre-medication with 10 milligrams of Valium and procedure dose of 9 milligrams of Versed. That combination, was negligent and was proximal cause of her respiratory arrest causing her anoxic encephalopathy (brain damage form lack of oxygen).
When a person is sedated and lying on their back (supine) you can easily observe their respiratory rate and depth of respiration. But on their stomachs (prone) these observations are more difficult to make and require a higher degree of diligence, which was not given, and also was negligent.
Furthermore, in the prone position there is the added problem of the extra weight of the body compressing the chest, impairing motion of the bellows effect of the ribs. Furthermore, the prone position also puts greater pressure on the abdomen which pushes into the diaphragm (breathing muscle separating the abdomen from the chest and serves as a “piston” to aid breathing).
They failed to properly protect this very heavily sedated patient who was now placed in greater danger in the prone position. She was overweight. The body fat is more inert than muscle for measuring lean body mass for the safest drug dosage calculations. Overweight people have a liver enzyme deficiency which makes them even more susceptible to the side effects of drugs.
They will try to claim that she herself turned to the prone position at their request, so how could she be overdosed? They gave her another intravenous injection (and ? more) after she was prone, per the note of Dr. O himself. Furthermore, the respiratory depressant effect can be overcome by sensory stimulation such as being told to turn over and aided during that maneuver (take depositions of all the operating room personal on that and all the matters of fact). Then prone she was further sedated and compressed by her own body weight, aggravating the respiratory effect of those potent drugs.
The anesthesia record notes that she had spontaneous respiration (“SR”) until 1:40 when she had controlled respiration (“CR”) from the endotracheal tube intubation. But the depth and quality and rate of her respiration was never noted. Shallow respiration is typically seen from excessive respiratory depressant drugs, and the carbon dioxide build up in the blood serves as a further respiratory depressant. She had nasal oxygen at 3 liters per minute during the surgery it may have become dislodged when she was prone.
They note that she had a blood oxygen monitor ongoing with her blood at 99 percent saturation during the operation until it dropped to 70 at 1:30. At 70 percent, it would not cause an arrest. It probably had no low level alarm on that device, or the alarm was not turned on or it was defective. Investigate that issue. Was there a product liability issue here, too?
When they noted her low heart rate she was given the drug Atropine to speed up her heart rate. That is negligent in an otherwise healthy adult. It delays what is needed with is mechanical mask-bag positive pressure ventilation. Who gave her the Atropine, why and exactly at what time, was that before or after they began positive ventilation when she was turned on her back? Did they first try mask-bag (Ambu) ventilation before Dr. O intubated her? No delay in positive pressure ventilation is acceptable.
I want to point out that after they intubated her a measurement of the expired carbon dioxide air (in the exhaled air) was not elevated, but it takes only a few deep ventiliations to return that to normal. This does not refute her respiratory arrest as the cause of her brain damage.
Also, at Hospital F.T. they erroneously noted that one of the anesthetic agents was the drug Ketamine. She never received this anesthetic.
In essence, they overdosed her with a combination of Versed and Fentanyl after pre-medication with Valium. Then they failed to monitor the quality of her sontaneeous ventilation after she was compromised in the prone position. Then they delayed her resuscitation. All that was negligent and the proximal cause of her permanent and irreversible brain damage.
Obtain all information on the Anesthesiologist and his Nurse Anesthetist: any previous problems, details of their training, business relationship and contracts.
I would recommend authorizing our office to obtain a Board Certified Medical Expert in Anesthesiology and obtain a Nurse Anesthesia, plus Board Certified Medical Experts in Pharmacology and Neurology if causation defense confabulations are attempted to be raised by the defense.
The Medical Review Foundation, Inc. remains available and ready to continue assisting you with this important case.
Back to Top
Patient With Pnemonia on a Ventilator Removes Endotraheal Tube; Negligent Reinsertion causes Lack of Oxygen and Death
At age 53, he was hospitalized on 6/28 with acute left lobar pneumonia that was determined to be caused by the germ Legionella, and he received proper therapy through consultations with specialists in Infectious Disease and Pulmonary Disease.
Because of his use of steroids to treat his rheumatoid arthritis, and a 35- or 50-pack-year history of smoking, he was more susceptible to this infection, and was more resistant to treatment. It was a judgment call, because of his worsening respiratory failure, to intubate him (insert an endotracheal tube via his mouth into his trachea: windpipe). This was done on 6/30 with a size 8.5 tube, which is for an adult male size.
The endotracheal tube has a balloon cuff surrounding the lower inch, which, when inflated, seals off the space between the tube and the inside of the trachea. This permits positive pressure from the ventilator to be directed into the lungs and not leak (dissipate) around that tube. It also prevents gastric fluid or feeding aspiration into the lungs. Through the tube, the nurses frequently suction secretions, and a bronchoscopy (use of a flexible fiberoptic tube) can be passed for diagnosis and suctioning mucous plugs that obstruct the bronchial tubes (branches of the trachea).
Some Hospitals may still recycle endotracheal tubes by sterilizing them. That process can damage the balloon cuffs and increase the risk of leakage. New endotracheal tubes must meet good manufacturing practices and be constructed not to leak. You need to find out what brand and model tube was used, whether or not it was changed, or removed and reused with each of the two bronchoscopies, and through the Freedom of Information Act obtain all the information on leakage problems from the Bureau of Medical Devices of the F.D.A. (on Fishers Lane in Bethesda or Rockville, MD)
Neurologically he was intact until the cardiac arrest caused by lack of oxygen (anoxia) and low oxygen (hypoxia), which occurred on 7/13 when at 1320 the Nursing Staff notified Dr. #1, that the endotracheal tube (ETT) was leaking. “Dr. #2 was notified and re-intubations with a new tube was planned.” With the leak, the PO 2 (pressure of oxygen in the arterial blood) was 80 and the percent saturation of the hemoglobin pigment in the red blood cells, which carry the oxygen like a sponge, was excellent at 97%. If the PO 2 drops below 70, the percent saturation will rapidly diminish. That did not happen with the leak, and although there was some urgency to replace the tube, it was not an emergency.
What is the expertise of Dr. #2 in urgent bedside intubations? He was consulted on 7/13 by Dr. #3 concerning the potential need for a tracheostomy (to be performed by Dr. #4). Did he do both attempts? Who inserted it at the arrest?
Why did they not arrange for an Anesthesiologist to remove the leaking tube and insert a new one? What became of the evidence: the leaking tube?
At the time of re-intubation, the patient’s muscles were “paralyzed” with the drug succinylcholine. That prevents all spontaneous breathing and he could not move. All his muscles, including his jaw and throat would be flaccid. He could not resist their efforts. But he could feel their probing his throat, and also experience the oxygen deprivation and any associated fears of dying, until he passed into permanent unconsciousness during the second attempt at intubation. He was sedated with Versed.
After the first failed attempt, “they” ventilated him with the venti-mask bag ventilator (by hand). The second attempt failed and during that prolonged failure, his oxygen level dropped to a life threatening level of 23% saturation. His heart was directly affected by too little oxygen and it slowed to 30 b.p.m. (beats per minute). He needed immediate oxygen and was negligently denied it. Instead, “they” gave him the drug atropine to speed up the heart rate. That was a serious error, since it was not slowing from a drug treatable condition. Muscles cannot pump without oxygen. The heart is a muscle. And after three to five minutes of too little oxygen, the brain will sustain irreversible damage.
We are taught to hold our own breath during intubation attempts so that we know when to desist and reventilate with the mask bag unit. In fact, the patient can be continuously ventilated until a more skilled Doctor arrives to intubate. Also, he could have been continuously ventilated until the planned tracheostomy operation could have been rescheduled to be done at that time.
All those failures were negligent by Dr. #2, Dr. #1, and any other involved staff. To persist in attempting intubation for 10 minutes while the patient cannot breathe from the paralyzing drugs and was on an oxygen monitor showing severe oxygen deprivation is clear negligence.
That directly caused his irreversible brain damage, documented at the autopsy on 7/28 (he died on 7/26 after his “advanced directive” was honored).
Dr. #5 explained the tracheostomy at (?) 1300. A Nurse called Dr. #2. Versed (a potent Valium-like sedative) was given as 5 mg each dose at 1345, 1347 and 1350 followed by succinylcholine intravenously at 1352. The “Code Sheet” noted Dr. #2 and Dr. #1 were present. The arrest occurred at 1400 and CPR began at 1400.
At autopsy, the severe left lung pneumonia was documented, as well as the diffuse damage caused by prolonged ventilator use. He was “dependent” on the ventilator, until his pneumonia would have begun to resolve. A patient cannot effectively cough on a ventilator, so suctioning, pulmonary physical therapy, and periodic bronchoscopies were used and would have been needed, until the lung condition improved.
Of the three coronary (heart) arteries, the least significant, the right coronary artery had an 80% (narrowing) stenosis, the left anterior descending had only 50% (not hemodynamically (blood flow) significant) and the circumflex artery was normal. Therefore, he had no significant coronary artery disease to otherwise shorten his longevity.
- - - - - - - - - - - - - - - - - - -
The Defense will argue that his Legionnaires’ disease pneumonia would be fatal after two weeks of antibiotics and ventilator use. I do not believe that to be true. Infectious Disease and Pulmonary Disease Experts could review the chest CT scan and x-rays (copies) and all these records to give you their opinion to the “so what” defense.
Based on the above, the Hospital and Drs.#1 and 2 departed from the accepted standards of care and caused his preventable brain damage and death.
As you follow up on my questions and suggestions, I suggest you authorize the Medical Review Foundation, Inc. to obtain Board Certified Medical Expert reviews in Infectious Disease, Pulmonary Disease, Anesthesiology, and Intensive Care Nursing.
Back to Top
Post–Operative Narcotic Drug Overdoses Causing Respiratory Arrest, Brain Death and Death.
According to the records, the patient was described as morbidly obese. She was 4 feet 11 inches in height and weighed 152 pounds. Much of this was fat, and her muscle mass and organ size, which would be responsible for the metabolic destruction and elimination of medications, including the narcotic medication, morphine, was certainly that of a small, elderly woman at age 72. Elderly patients are much more sensitive to the effects of narcotic medication, including the well-known respiratory depression effects of that type of drug.
The patient had known lung disease. She was a heavy smoker, smoking five packs a day for many years, and then cut back to a half a pack a day. They believe, and I agree, that the heavy cigarette smoking was a substantial proximate causation of her kidney cancer.
Her lungs were not normal. Prior to surgery on room air, she had a measurement of her oxygen capacity and pO2, the partial pressure of oxygen within the blood, that was only 65. Although the oxygen saturation was 96%, the hemoglobin will suck up and hold on to oxygen quite readily. But when the pO2 is at 65%, only a small drop of another 10 pressure points will totally drop the saturation curve down dramatically and put a patient in grave danger.
Furthermore, the anemia that the patient had decreased postoperatively down to a hemoglobin of 8.2 (with a normal range of 12.4-15.2) and a hematocrit (the packed red blood cell volume) of 25.8 (with the normal range of 36.7-45.1). This meant that postoperatively the ability of her blood to carry oxygen throughout her body was at approximately only two-thirds of normal. Thus, there was a lowering of the oxygen content within the blood, and with the anemia level showing that her blood could not carry a normal amount of oxygen into her body, these would both contribute to a potential fatal outcome.
The patient developed painless, bloody urine and her physician correctly obtained a intravenous polygram (kidney x-ray dye study) which showed a probable cancer of the kidney. This was confirmed by the CAT scan and then by the cystoscopy examination and evaluation. Thus, the radical operation that was scheduled and performed on this patient by Dr. #1 on January 2 the radical left nephroureterectomy (removal of the kidney and the adjacent flesh, including the adrenal gland and the ureter) was clearly indicated.
My review of the detailed operative report shows that the patient was placed under general anesthesia, and after the correct operation to remove the kidney with the cancer and the adjacent flesh, a separate incision was made in the lower abdomen to excise that specimen along with the ureter as an intact specimen. All this meets the standard of care.
The Pathologist confirmed that the patient had a grade I-II papillary transitional cell carcinoma, and that the cancer was confined to the kidney. This is a low-grade cancer that had not had any evidence of metastatic spread, and thus this patient had a high chance of a cure, particularly considering her age at 72.
According to the anesthesia record, the patient had a pulse oximeter measuring her blood oxygen level, and the safeguard measurement of expired carbon dioxide confirmed that there was no dislodgment of the endotracheal tube or the connection between the ventilator and the endotracheal tube during the anesthesia. The patient was generally reasonably stable and I find no fault with the actual operation itself, or with the anesthesia performance.
Postoperatively, the patient was admitted to the postanesthesia recovery room in basically an extremely stuporous condition, and shortly thereafter as the minutes began to pass, she began to awaken. During that time, to control pain, the patient did receive injections of the narcotic medication, morphine.
Generally speaking, an elderly patient at age 72 who was actually a small person in a fat body, in my opinion, should not receive more than 1-2 mg of morphine every two to four hours. The morphine given to the patient must be to control pain, and only when the patient has pain.
In the recovery room, the patient received her first dose of morphine, 1 mg intravenously, at 17:42, and through 18:20, received a total of 8 mg of morphine as well as 30 mg of the non-narcotic pain medication, Toradol. This is a lot of morphine and the patient, who was awakening initially, was noted to have very shallow respirations at 19:30, at the time she was discharged from the recovery room. This was an ominous sign.
When she was admitted to her regular hospital floor and bed from the PACU, she was noted to be lethargic. She opened her eyes and was trying to get out of bed and thus was obviously quite confused. This confusion is not pain. I have not seen the doctor’s orders to determine who, in fact, actually ordered the PCA (Patient Controlled Analgesia), which is a button the patient pushes that allows a special calibrated pump to inject narcotic medication, in this case, morphine, into the intravenous line. The calibration adjustments are determined by the Physician’s order and set by the Nurse. Thus, when the patient has pain, the patient pushes the button and get a dose of narcotic medication.
Usually, the Anesthesiology Department is in charge of the PCA orders and machine, but this can vary from hospital to hospital. I cannot tell who ordered the medication or which Physician was responsible for monitoring the dosage given to the patient at the Hospital #1.
According to the records, the patient had very poor eyesight. At 21:30, she opened her eyes. The respiratory rate was 16. The PCA was being used for pain control as noted in the nurse’s notes. She was receiving 3 liters of nasal oxygen, and the pulse oximeter on 3 liters of oxygen showed that her percentage of saturation of oxygen in the blood was 97%.
After midnight on January 3rd at 00:05, the patient was noted to be very lethargic and not responding to verbal stimuli or pain. If she was not responding to verbal stimuli or pain, why was she still receiving dosages of the narcotic pain medication? Obviously, a lethargic or stuporous patient would not be pushing the button. Who was pushing the button all this time because throughout her entire stay until the respiratory arrest that caused the cardiac arrest, she was noted to be lethargic or stuporous and still was getting pain medication.
At 01:30, she remained lethargic, only opening her eyes, but they had a glazed appearance. At 02:20, the patient said yes, but not in response to any question, and she was lethargic. At the time that the number appears to be blocked but looks like it ends in a 45, so it was either 04:45 or 05:45, it was noted that the patient had a leg in the bed rail and was repositioned. Then it says, “PCA pushed for patient,” by a Nurse or Nursing assistant who appears to be #1. In my opinion, that is a negligent act. Why would a Nurse or Nurse’s aid push a button of a patient on narcotic medication other than to basically have them more easily controlled? That is not the purpose of the PCA machine in giving the patient pain relief, and stuporous patients are not in pain. This act defies any rational basis in my mind.
The patient remained lethargic, including at 8:40 in the morning and throughout that day. At 17:00, she was noted to be lethargic at times. She was resting. At 19:00, she was noted to be resting comfortably. This was from the Nurse’s aid. Thirty minutes later at 19:30, (7:30 p.m.), the family yelled for “help,” and that “she is not breathing.” They found the patient without respirations, cyanotic (blue from lack of oxygen) and pulseless.
How mush delay was there? What occurred before she stopped breathing? How shallow was her breathing? Cardiopulmonary resuscitation was immediately started and I have no concerns with regard to the adequacy of that process. However, the patient was without oxygen for such a long period of time that she ended up with severe brain damage (hypoxic encephalopathy). A number of EEG studies (brain wave studies) performed after the event and over the ensuing months were all consistent with that finding. In addition, the patient had a CAT scan on January 5 that showed no evidence of any hemorrhage or other abnormalities. An MRI was performed on January 9th. Again, there was no evidence of any mass, mass effect or hemorrhage. There were no other mechanical problems in the brain. Another CAT scan on January 23rd showed that the brain was within normal limits. That is, there was no evidence of any hemorrhage or abnormality within the brain to cause the patient’s brain to be damaged.
All of the above is consistent with a gross overdose of narcotic medication (morphine) given repetitively to a stuporous and lethargic patient by negligent orders by the physicians not terminating the PCA machine and by the nurses actually pushing the button at least one time. The doctors in their progress notes questioned who was pushing the button. The family denied pushing the button giving the stuporous patient more pain medication.
In any event, the order should have been changed to stop the PCA machine, or at least to drop it back to 1 mg of morphine, not every hour, but every two or three hours as needed, or to stop the PCA machine and give the patient injections of pain medication as had been done for many years upon demand when, in fact, the patient needed pain medication and was not in a stuporous state.
The Hospital Patient Controlled Analgesic (PCA) flow sheet is most informative. She was receiving morphine sulfate (MSO4) initially at 2 mg per dose, and then sometime on January 3rd, with the time not stated, was decreased to 1 mg with 10 minutes of lock out. This would allow the patient to receive 6 mg of morphine on an hourly basis. This is a gross overdose for a 72-year-old woman who is of very small muscular and skeletal stature.
I want to point out that I was shocked to note that on this sheet, as of 6:30 in the morning on January 3rd, she had received 11 mg of morphine and until 19:00, which is 7 p.m., she received 25 mg. Thus, in the twelve and one-half hours between 6:30 in the morning and 7 p.m., she received 1.12 mg of morphine per hour. This, in my opinion, is a significant overdose for such a small patient of age 72. But more importantly, she did not need this pain medication. The patient was narcotized; that is, she was receiving a continuous gross overdosage of narcotic medication when she was continually stuporous. The first thing to consider in a patient who is postanesthesia who is still not waking up to the extent that one would want is to stop the pain medications.
I also wanted to point out that by 15:20, she had received 23 mg of morphine through the PCA machine. But, from 15:20 until 19:00, she received another 2 mg. Why was she receiving all this narcotic medication when the record shows the patient was not in any pain? She was resting very quietly, but that quiet resting was actually substantial oversedation from the narcotic medications. All of this is negligent care.
The patient was also receiving an antipsychotic medication which, to some degree, can also cause some sedation, but, in my opinion, the clear negligence is in giving a stuporous patient, a patient who is not in pain, narcotic pain medication. She could not push the button. Who was pushing the button? How did she get all these high dosages throughout the night? Was there someone sitting by her bedside pushing the button throughout the night, and why do the Nurses’ notes show that, in fact, a Nurse or Nurse’s aid actually pushed the button for the patient when the patient was stuporous or lethargic. This is not a patient who needed pain medication.
This was a patient who needed a doctor to stop the pain medication to allow the metabolic effect, that is, the stuporous effect of the narcotic and the excessive sedation of this patient, to terminate for many reasons. Patients who are so stuporous cannot effectively cough and clear their airways. They can choke on food and on liquid. Such patients will be breathing shallowly. There are times she had shallow respirations. Such a patient will eventually end up with an accumulation of the narcotic within her body and the effect of respiratory depression to such an extent, and particularly as her anemic state progressed and became worse, in a patient who had chronic lung disease to start with wherein it would all combine to basically kill the patient. To kill patient by stopping her breathing.
I cannot tell from these records whether or not the oxygen, that is the supplemental nasal oxygen of 3 liters per minute, was on in a continual, ongoing basis. This will have to be clarified through discovery. However, giving a patient nasal oxygen where they are so overdosed with a narcotic that the respiratory center is so depressed will not keep them alive. You cannot give enough nasal oxygen to a patient. They need to be placed on a positive ventilator to actually force air and oxygen into their lung, but in this case it would have been so simple to just stop the narcotic for a period of time and give the patient an adequate dosage to relieve the pain, but not to overly sedate her and not to place her into the great zone of danger through which all of the negligence of the Nurses and of the Physicians combined to cause her to have a respiratory arrest that stopped oxygen through her entire body and caused her heart to temporarily stop. They were able to restart the heart, but the brain is much more sensitive to oxygen deprivation, and after three to five minutes of lack of oxygen, one would have a patient who, in this case, had severe and irreversible hypoxic encephalopathy; that is, brain damage from lack of oxygen. The subsequent CAT scans and MRI studies, as well as the EEG studies, were all consistent with this finding. There is no other cause of this condition.
In addition, the patient did not sustain a pulmonary embolism. As for the traveling blood clot from the leg or pelvic veins to the heart-lung circuit as a cause, the findings here are not consistent with that, and in fact, she had a lung scan study a number of weeks later that showed no evidence of any pulmonary embolism. Pulmonary embolism in an acute postoperative period would be quite unusual in any event. All of the above, in my opinion, was related to the negligence of a gross overdosage on an ongoing basis in this patient to the point where it overwhelmed her, stopped her breathing and caused her to have irreversible brain damage, which was the proximate cause of her eventual death.
I would suggest that you authorize us to have Experts review these records, who would be Experts in the field of Nursing and in Anesthesiology. You also need to determine who, in fact, was responsible for the PCA narcotic orders, and because the patient was also treated by a Urologist, a Urologist as a Surgeon would be responsible also for seeing the patient and determining what would be necessary to benefit the patient, which, in this case, would be to read the medical orders and stop the narcotic pain medication until she awakened, and call any consultations as necessary.
Back to Top