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Diabetic Ketoacidosis Inadequately Treated Resulting in Obvious Deterioration and Respiratory Cardiac Arrest
This case concerns the care and death of this 33-year-old female insulin-dependent diabetic.
She was seen in the office of Dr. Chuck on 9/26 for a reasonable diagnosis of bronchitis and he prescribed an antibiotic (Biaxin). She had a history of recent fever, a cough and chest pain with coughing. Her respiratory rate was not recorded, but she was not noted to be short of breath. The chest was clear. No rapid heart rate was noted. Based on all of the above and the subsequent finding of a normal chest x-ray on 10/1, I can find no fault with his office care.
When she called his office on 10/1 at 11:25 a.m. with intractable nausea, vomiting and diarrhea, she was referred promptly to the Emergency Room and they were notified she was on her way there. She was immediately seen at 14:11 and was correctly cared for by Dr. Olly. The laboratory tests revealed diabetic ketoacidosis (blood sugar of 477, which is four times normal), ketones in the urine, acid blood, dehydration with concentrated urine, and BUN (acute kidney test) elevated with the more chronic kidney blood test, creatinine, normal, and concentrated blood with the hematocrit elevated at 50.2. This was a dehydration from her acute illness.
Her blood was dangerously acid with the pH at 7.05 (almost lethal level), and she had compensated to raise it “that far” by eliminating as much carbon dioxide from her blood as possible by hyperventilating (the PCO 2 was 9 with the normal range being 35-45). Also, she used up almost all the bicarbonate in the blood by trying to buffer (neutralize) the excess acid with it at 2 (normal is 22-26). All this gave her a negative base excess of –26.4 with the normal of –2.0.
All this means she needed lots of fluids to rehydrate her and lots of bicarbonate to return her almost lethal blood and body acid status to normal or at least near normal, and enough as tests continued to reveal defects.
She received adequate fluid at 500 cc (17 ounces) per hour, and after she had produced more than one liter (quart) of urine, it was reduced to a generous 250 cc per hour. Her hematocrit came down to a normal 42.5 by 5:55 a.m. on 10/2. Her blood sugar dropped to below 200 at midnight and remained in a safe diabetic range thereafter.
However, no one checked her arterial blood gas level (other than oxygen, which was fairly normal). No pH or PCO 2 levels were ever tested again, despite the persistently very abnormal venous blood bicarbonate values of 5 at 1508, 4 at 21:30 on 10/1, and 8 at 0200, 0555 and 1000 on 10/2. That failure to respond is somewhat ominous. In my opinion, the failure to recheck her arterial blood pH (and PCO 2) was a departure from the accepted standard of care.
Her in-hospital care was given by Dr. Maddy. He wrote most of the medical therapy orders. Dr. Liddy wrote orders at 1225 (9:25 p.m.) on 10/1 and 0305 on 3/2. Dr. Maddy ordered more bicarbonate to be given at 2225 by IV “push” and to be in her next intravenous bottle and “call next chemistries 7 (which includes the blood bicarbonate) results to Dr. Liddy.” That test was at 0200 on 10/2 and the value was very low at 8, as I noted above.
An insulin-dependent diabetic in diabetic ketoacidosis is very fragile. In my opinion, even though she was responding to her rehydration and insulin therapy and feeling somewhat better, they departed from the standards of care in not more closely following her acid blood condition and more frequently giving her more adequate doses of bicarbonate to correct her dangerously low and persistently low blood bicarbonate (acid buffer).
At 0915 on 10/2 the respiratory rate was at the upper limit of normal. At 1015 it was 27. At 1115 it was 30. At 1215 it was 55. Her hyperventilating to “blow off” carbon dioxide (acid) had markedly increased, but no one ordered any repeat arterial blood gas values (especially the pH), since the blood oximeter only measured her oxygen in her blood, which was adequate, although it should have been higher considering the fact she was on supplemental nasal oxygen.
They were watching but not interceding. That is negligent, especially since they knew her blood bicarbonate buffer was too low and with increasing hyperventilation from her decompensating acidosis, her mental state (from alert to coma) was predictable, and that put her at greater risk of aspirating (choking) on her vomitus and arresting.
The Respiratory Therapist could not finish her ordered therapy (why??), walked out of the room and she promptly arrested.
The Nurses noted that at 1005 she “complained of shortness of breath (SOB) “and her respiratory rate in mid twenties to mid thirties.” She was “anxious.” At 1020 she “developed expiratory wheezes and appears more labored in her respiratory effort,” and “Dr. Maddy has ordered a respiratory treatment and a chest x-ray (CXR).” It was performed at 1040 and at 1125 “revealed a white out of patient’s right lung. CT ordered” which she initially refused when initially presented at 1059 by a Pulmonary Specialist, Dr. Bunt, even though he told her that her lung condition was life threatening. She said: Well, that’s too bad.” He did not order urgent repeat arterial blood gases, even though it was in his specialty. He focused on the CT scan and bronchoscopy intervention (which earns him a fee and was indicated), which she refused.
His failure to order that urgent blood test is a departure from the standards of care, particularly when the Respiratory Therapist noted that her respiratory rate (RR) was 55, three to four times normal, and she was in respiratory distress. Also, he should have had the Anesthesiologist see her at that moment to electively intubate her and put her on a respirator (ventilator).
At 1140 her RR was 42 and she was “visibly labored.” She was found “nonresponsive, RR labored, irregular and decreased from previous – now in the teens.” She was going into an arrest before their eyes. At 1202 the Respiratory Therapist began positive pressure mask ventilation (bagged), the Anesthesiologist was called at 1204 to inert an endotracheal tube but despite sedative (Versed) and muscle paralyzing drugs ( succynlcholine) with two doses (20 mg and then 80 mg) her mouth could not be opened. The she was given a curane drug (Nucuron) and that released her teeth clenching jaw spasm, but he could not intubate her windpipe. This can be very difficult in an obese woman, 200 pounds in a hospital bed under emergency circumstances.
A Surgeon, Dr. Giddy, was called at 1220 to perform a tracheotomy to cut into her windpipe to insert a tube, and because of her obesity, that was not successful (but she was ventilated with the mask/bag ventilator). He tried to inert a needle into the cricothyroid membrane and again it was not successful. All of his care is not negligent, nor was the Anesthesiologist negligent under these circumstances.
She was pronounced dead at 1252 by Dr. Maddy.
The sudden change in her right lung was either a very large pleural effusion (fluid outside the lung between it and her ribs), or acute pneumonia-like changes. The central venous pressure catheter, if it punctured the vein and entered the lung outer space at the insertion, followed by all that fluid could cause that effusion. However, they were able to withdraw blood from the needle tube confirming its intravenous position. The chest x-ray showed it to be anatomically in the vena cava (large vein), and her body received the fluid because over her brief hospitalization she produced more than two liters of urine.
So the x-ray change most likely was from acute aspiration in her very ill state, which risk was significantly increased by their negligent failure to carefully retest her blood pH and give her adequate amounts of bicarbonate as her body required, not just “flying blind” or worse, doing minimal therapy in spite of her persistently dangerously low blood bicarbonate (acid buffer), which is a simple venous blood test done in a few minutes, her respiratory distress, and severe aspiration pneumonia-like acute changes.
In my opinion, if they adequately treated her acid state after she was admitted to the hospital, she would not have aspirated (and therefore also eliminated much of her lungs’ ability to “blow off” the acid carbon dioxide), and simultaneously damaging body (lung) flesh, increasing her acid production.
Was an autopsy done? If so, obtain the complete report.
The blood culture tests were negative for germs (sepsis), but the sputum culture laboratory test result is missing. It is important to see if she had lung germs (even with the initial negative chest x-ray), because I do not find that she actually received any antibiotics other than 2 grams of Rocephin intravenously at 1620 on 10/1 in the ER. So it may or may not have made a major differences in the context of all her care and death.
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The Defense will argue that she was “getting better,” her blood sugar and fluid hydration levels were very acceptable and she refused the CT scan and bronchoscopy (which probably would not be done before she died anyway). One record noted that she had a BKA (below the knee amputation), which could show how precarious she was for longevity. Did she have a leg amputated, and if so, why? Since she was hospitalized two years before for pneumonia, it is important to obtain those records for review to see how it may impart on this occurrence. She also smoked cigarettes. Who made what efforts to get her to stop, especially since she had pneumonia two years before? And who made what efforts to get her to lose weight, which makes her diabetes easier to control and aids breathing ability?
I would suggest that you authorize the Medical Review Foundation, Inc. to have all the records (including the requested ones) reviewed by Board Certified Medical Experts in: Endocrinology, Infectious Disease, Pulmonary Medicine and Critical Care/Intensive Care Medicine.
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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.
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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.
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Head injury patient given anticoagulation (blood thinner) for heart attack concern; develops cerebral hemorrhage, coma, and dies.
The basic standard of care in medicine requires the doctor to take an adequate medical history, perform a reasonable physical examination and create a "differential diagnosis," a list of probable diagnoses based on the history and physical. This differential diagnosis is the fundamental basis of all medical and surgical care, and is taught to every third-year medical student. They then have to rule them out and not endanger their patient.
In this case, a 65-year-old diabetic man (for 25 years) had a history of coronary artery heart disease for which he had a coronary artery bypass graft (CABG) operation two years before and amputation of both legs because of severe artery disease that did not respond to vascular surgery.
He was taken by ambulance to the emergency room on April 24 complaining of "tightness in the chest and shortness of breath (SOB) for a couple of hours with vomiting and dizziness."
He told the Emergency Room Triage Nurse, "Two days ago fell out of wheelchair and struck back of head on concrete. Last p.m. onset of SOB plus vomiting x 3, followed by chest pain and continued SOB." At that time (0625), he "denies any chest pain. Complains of SOB…" The lungs had "fine rales," which are wet breath sounds consistent with congestive heart failure, also confirmed by a chest x-ray.
Just before he was admitted to the Coronary Care Unit, the emergency room nurse's note begins with, "…History of (H/O) fall out of wheelchair, striking back of head on concrete."
The nurses admitting physical examination form states under "skin": "abrasion (scrape) noted back of head from recent fall, tender to touch. Nurse #1."
Dr. #1, his regular physician, saw him and failed to note anything about him falling and striking his head on concrete. One of the causes of vomiting is a head injury, especially where there is bleeding or swelling involving the brain. The failure to obtain that relevant "present illness" medical history (or to simply read the emergency room record where it is recorded in two places) is a departure from the accepted standards of care.
Dr. #1 also performed an inadequate physical examination because under "HEENT (head, eyes, ears, nose and throat)" he noted, "hearing aids, normal fundi (retina: back of the inside of his eyes, which is unlikely in an insulin dependent diabetic of 25 years duration, since they develop multiple areas of small blood vessel [artery] disease) and thyroid normal…." Not one word about the tender abrasion on his scalp.
Having failed to obtain (or read) the relevant head injury history, or note the head injury with his physical examination (both negligent), he jumped to the conclusion that he may be sustaining a heart attack. The EKG (electrocardiogram) was not supportive of that diagnosis. The cardiac enzymes (CK-MB: creatine phospho-kinase myocardial band fraction), which are proteins released into the blood from oxygen starved and dying heart muscle showed "slight elevations of the CK-MB fraction." (Normal is 0-5.0. At 7:05 a.m. in the Emergency Room it was 7.09 and at noon it was 6.91.) This is questionable and it did not rise, even more questionable.
If there is any reasonable potential for a head injury that caused bleeding within the skull (brain), a CT scan done as an emergency is the proper standard of care before any anticoagulation ("blood thinner") is started. Dr. #1 failed to obtain a CT scan because of his negligence in his differential diagnosis, noted above. He ordered STAT (now) grains V (one adult 325 milligram aspirin) and it was given at 0855. Aspirin will damage all the platelets (clotting particles produced by the bone marrow) and will have its effect for up to one week, until the body makes enough healthy undamaged new platelets, or they are given by transfusion.
To make matters even worse, he ordered the very potent injectable anticoagulant, heparin, to be given intravenously (IV) as 5,000 units immediately and then 1,000 units IV every hour. He ordered the blood coagulation test for monitoring its "therapeutic" effectiveness, the PTT (Partial Thromboplastin Time). At 1040 on April 24 the PTT was 23.2 with the normal range of 25-35 seconds, but at 2100 it was 51.6 and on April 25 at 0600 it was 46.3. It was working.
By 1430 on April 24, he had already received the 5000 units of heparin and was getting the 1000 units per hour. He was "awake/alert/oriented." At 2300 he had "fleeting nausea without emesis. Medicated with Tylenol for headache and leg pain...." Dr. #1 was made aware of all the laboratory results but the failure of the nurse to advise him of the patient's headache, considering all of the above, was a departure from their accepted standards of care.
At 2300 he was found "lethargic, diaphoretic (sweating), BP (blood pressure) 170/100 (elevated even for him and it rises as the pressure in the brain rises). C/o (complains of) severe frontal headache." They also noted a change in his sensorium, "disoriented to time and place…follows commands but stares blankly when asked where he is - only verbalizes re: my head hurts very badly - Dr. #1 called - advised regarding patient's complaint of pain, headache, increased BP (blood pressure), neuro (neurological) status - apparent confusion - orders received for Tylenol with codeine (a narcotic) for headache to be administered. Nurse #1."
He is grossly negligent. His patient receiving therapeutic doses of a "blood thinner" had a severe headache and significant neurological change. Even if he never knew of the head injury, the standard of care demands that the heparin be stopped, the antidote, Protamine, be given, a physical examination by some doctor (him, a Neurology or Neurosurgeon consultant, or even the Emergency Room Doctor) be done without any delay, and an emergency CT scan be done. It would have shown early bleeding into his brain and had a reasonable chance of not bleeding further with his clotting mechanism impaired by the heparin anticoagulant all night long, if he was treated with the antidote. He may not have had any significant defect and would not have died.
The Nurse was negligent for not going to her supervisor (up the hospital "chain of command") to protect her/their patient from obvious (to a nurse) negligence (even if she did not know of the head injury in the nurse's notes in the chart in front of her).
At 0030, "Patient complained of headache (c/o HA) - medicated with Tylenol with codeine grain ? (15 milligrams)." The heparin was running well at 1000 units per hour. During that 11 p.m. to 7 a.m. shift, "Patient lethargic but arousable (illegible words)."
By 8 a.m. he was "not responsive" and the heparin was turned off, but no antidote given to immediately stop its lingering effect for a few hours. Further negligence.
At 9:20 a.m. on April 25 he was transported for the CT scan of his brain which showed blood on both sides of its surface and within its flesh. A neurologist and neurosurgeon were called to see the patient and gave proper care. There was no localized area of blood (hematoma) to operate on and drain. The next day it was somewhat more as blood degenerates and increases in its volume and damage to his brain. He was comatose. They tried to decrease the swelling with a potent steroid medication (Decadron) and diuretic that pulls water out of the brain (Mannitol), but he died in a deep coma on April 28.
Because of initial findings of congestive heart failure (CHF), Dr. #1 correctly ordered the very potent diuretic Lasix. However, it helped to somewhat dehydrate the patient and caused a reversible type of kidney failure (pre-renal azotemia). That part of the care was not negligent, but the cause of death on the death certificate assigned by Dr. #1 as, "Part 1 (A) Immediate cause: Acute renal (kidney) failure; due to or as a consequence of: (B) Chronic renal failure; due to or as a consequence of: (C) Diabetes mellitus; other significant conditions contributing to death but not related to cause given in Part 1 (A): Heart failure, ASHD (arteriosclerotic heart disease), cerebral hemorrhage," it is negligent and a cover-up.
That is grossly wrong and a falsification of the death certificate. He died as a direct effect of the unchecked cerebral hemorrhage markedly worsened by Dr. #1's negligent beginning anticoagulant therapy and not stopping it promptly when the nurse told him of all the factors that would lead any prudent physician to stop the heparin and intercede as I noted in detail above!
Dr. #1 and the Nurses (therefore the Hospital) were negligent as I noted, and their negligence was the proximate premature cause of the death of this patient.
In this case I suggest you authorize us to obtain the services of Experts in Neurosurgery, Neurology, the same specialty of Dr. #1 (what is his Board Certification and how does he advertise his services in the Yellow Pages?) and a Nurse.
The Defense will contend that he did not come to the Emergency Room complaining of a headache. He complained of tightness in his chest, the CPK-MB enzymes were "slightly elevated" and the chest x-ray was very consistent with congestive heart failure. However, he failed to take a recent medical history or even read what the nurses wrote. He was then called at night with all the information that a third-year medical student would be able to conclude: Rule out cerebral hemorrhage in a patient receiving therapeutic doses of a potent anticoagulant. He failed to act responsibly causing the death of his patient, which he covered up by falsifying the death certificate!
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