Please click on the titles below to go to the corresponding sample Case Evaluation Reports.

• Eighteen Hour Delay For Surgery For Leaking Abdominal Aortic Aneurysm Increased Risk Of Death. New!
  
  
• Baby with Meningitis Misdiagnosed as Bladder Infection, Inadequately Treated, becomes Deaf.
  
  
• Gun shot wound to the heart with collapsed lung and pericardial tamponade (clots squeezing the heart like a vice), emergency open chest surgery and failure to suture the two holes in the heart.
  
  
• Head injury after a seizure or beating with lethargy assumed to be from the seizure, no CT scan, and sent home with intra-cerebral hemorrhage causing brain death.
  
  
• Elderly patient with severe vomiting forced fed x-ray dye, vomits and chokes in a CT scanner, and delayed and improper rescusitation with coma, and then perforated stomach and surgery from medication errors, and followed by death.
  
  
• AIDS Patient comes to Emergency Room with pneumonia and needs a ventilator. He gets steroids, gets worse and dies.
  
  
• Diabetic foot infection mistreated resulting in gas gangrene and leg amputation.
  
  
• Head injury in an elderly patient taking an anticoagulant (blood thinner), not given antidote, resulting in brain hemorrhage.
  
  
• Not diagnosed heart attack and developing stroke was claimed.

Eighteen Hour Delay For Surgery For Leaking Abdominal Aortic Aneurysm Increased Risk Of Death.

This 71-year-old male Attorney who was in good health and no history of kidney stones or infection, developed severe abdominal and back pain of a sudden nature on 4/18 and was taken to the Emergency Room of the VA Hospital at 5:00 PM with a shocky blood pressure of 80/55 and no elevated temperature.

A physical examination would be required without delay.  He was not seen by Dr. Belinda until after 6:29 PM and NO ABDOMINAL EXAMINATION was done.  That it is negligent.  It would have revealed a pulsatile abdominal mass of a ruptured/leaking abdominal aortic aneurysm premises (AAA), totally consistent with a history, and the first priority to rule out in a differential diagnosis.  Dr. Belinda only noted in the “Diagnostic Impressions: Left lower back pain” without doing any abdominal examination, and not even considering the shocky blood pressure, again consistent with a ruptured/leaking AAA.

It was not until Dr. Brittney came on duty and saw him at 3:00 AM was that an abdominal examination was performed revealing the obvious "pulsatile abdominal mass," which at surgery measured 10.5 x 12.0 cm (one inch equals 2.54 cm), and was present before rupture for years.  The risk of rupture rises dramatically after 5 cm. 

Obtain all previous medical records and copies of all previous abdominal x-rays to determine if any previous Doctor was negligent in failing to diagnose it when it was in its chronic expanding state.  How much did the patient weigh?  How tall was he, and what was his belt size?  The thinner the patient, the easier it is to feel (palpate) the mass.  However, its size would not have changed significantly in the ER where any abdominal physical examination certainly should have revealed it at 6:29 PM.

The CT scan confirmed its size and location and the presence of an abnormally located right kidney (which was in his pelvis).  Dr. Brittney was notified of the CT results at 5:15 AM and it was also discussed by the Radiologist with “Dr. Blake from surgery.”

Surgery began at 7:30 AM and ended at 12:15 PM (4 hours and 45 minutes), and was complicated by the size of the hematoma, the need to ligate (sever and tie) to the left renal (kidney) vein for exposure.  The aneurysm was opened and replaced by a graft.  Because of the hours of negligent preoperative delay, there was swelling (edema) of his intestines, which prevented the suture closure of his abdomen.  The intestines were placed into a "Bogota Bag” and it was sutured to the large incision.  After days, the swelling would decrease, and he was reoperated upon on 4/24 to remove the bag and with the use of mesh, the incision was sutured closed.  He had been receiving various antibiotics from 4/19.

He developed kidney failure, required hemodialysis, became more ill, and the family agreed to a DNR (Do Not Resuscitate) order.  He died on 4/29 at 5:17 PM.  The details of the cause of death are not fully delineated, but they claim he developed “septic shock."  This is an overwhelming infection that damages all vital organs.  I found no blood culture (laboratory) reports (including any showing germs in his bloodstream or elsewhere.)  No autopsy was performed.

The hemodialysis (kidney machine treatment) was used to remove excess bodily fluid and correct the acid condition of his body, but apparently was not beneficial to his general condition, as it to was hoped it would be.

When a patient has their intestines in a bag (even with attempts of sterility), and then requires a second operation, the risk of infection increases.

The longer the delay while shocky before AAA surgery, the more damage will result, including increasing the risk of kidney failure (which is also a risk of the AAA surgery).  But in the Emergency Room records, I found no other recording and therapy for his shocky blood pressure.  (The Nurses notes are missing, as are all the Hospital Nurses notes and Laboratory Reports.)

In my opinion, if he would have been timely seen, correctly diagnosed, and operated upon, he would have been in the Operating Room within two hours of arrival and would not have required the second operation to remove the intestinal bag and close the incision.  All his risks would have been less, including the risk of infection and the consequences of sepsis.  His risk of dying would have been less than 10 percent, but all their negligence, including not treating his shocky state for hours, increased his risk of death, which in his case became 100 percent.

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The Defense will argue that a ruptured AAA is highly lethal.  That is true for all those who before after arriving at hospital.  They will argue that his left renal (kidney) vein had to be severed for operative exposure, and that put his left kidney at risk for failure.  But his right kidney was in his pelvis, and its vein was not sacrificed.  They will argue that the Surgeon had to clamp across the aorta above both kidneys to prevent hemorrhage and that temporary clamping could cause kidney damage and failure.

The Anesthesiologist, at the Surgeon's request, must give 25-50 grams of the osmotic diuretic, mannitol, before the aorta is cross clamped in order to decrease the risk of kidney failure.  With the right kidney known in advance (by the CT scan) to be in his pelvis, the aorta would have to be clamped at least above it to insert the graft I have not seen the anesthesia and Operating Nurses notes records, and if mannitol (or even the diuretic, Lasix) was not given before the aorta was cross clamped, both of them would also be negligent.

Obtain the personnel records of “Dr. Belinda” to see what, if any, problems she had before and after this patient's care.  Obtain her medical school, internship, residency and Board Certification (if any) records, as well as all of her licensing records too.

Obtain the Death and Complication records from the Hospital regarding this case.

The more than 14 hours delay is unconscionable and negligent and markedly increased his risk of death.

What details were the family given when they agreed to a DNR (Do Not Resuscitate) order?

The Board Certified Medical Experts the Medical Review Foundation, Inc. recommends in this case includes: Emergency Medicine and Vascular Surgery and they are available through our firm.  The Medical Review Foundation, Inc. remains willing, able and ready to continue assisting you with this important case.  We await your instructions to proceed.

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Baby with Meningitis Misdiagnosed as Bladder Infection, Inadequately Treated, becomes Deaf.

The records clearly show that this patient developed spinal meningitis and, secondary to that, had seizures and significant hearing loss. The hearing loss was on the basis of nerve/brain damage, not ear infections. I will discuss the care prospectively and point out areas of negligent care and what intervention should have taken place.

This patient was born on October 13, and was a full term pregnancy. The birth records reveal that she weighed 9 pounds 7 ounces and the Apgar scores were 9 out of a maximum of 10 at one minute and at five minutes. This is predictive of good neurological function. Up to age 6 months of age, she was performing according to appropriate standards. 

On April 25, she was seen Dr. #1. The left eardrum (tympanic membrane) was injected (inflamed). Her throat was also inflamed. He diagnosed otitis media (ear infection), pharyngitis, and dehydration, but she was sent to the Emergency Room for further evaluation and disposition. She was seen in that emergency room on April 25 at night, at 10:20. Her previous temperature was 102.5, but at that time, it was 104.3, her pulse was rapidly elevated to 164, and her respiratory rate was increased to 28. 

She was seen by a Physician whose name is not legible, and the patient had a complete blood count and urinalysis performed. They also took a sample of her blood to rule out the presence of germs in the bloodstream, which is called bacteremia or sepsis, and is a life threatening condition. Their first diagnosis was "fevers: rule out bacteremia" and the second diagnosis was "possible UTI (urinary tract infection)." In fact, he noted they sent a urine culture to the hospital laboratory and "in 1-2 days it will show us which bacteria caused the infection and if the prescribed antibiotic fights the bacteria."

The urinalysis obtained on April 25, evaluated in the Emergency Room, before the patient left, and noted by hand on the Emergency Room record, showed that there were only 0-2 red blood cells and 2-5 white blood cells seen under the microscope. There were no bacteria seen, and the dip stick of the urinalysis for the "leukocyte esterase" was "negative." This is strong evidence against a bacterial infection, in addition to the negative findings of the microscopic examination I just described.

Based upon all of that, in my opinion, this patient did not have a urinary tract infection (UTI). With a fever of 104.3, plus the rapid pulse and respiratory rates in a patient under these circumstances, in my opinion, she should have been seen by a Pediatrician or the Emergency Room Physician should have also performed a spinal tap. When patients have findings that are not consistent with the laboratory tests and physical examination for the presence of elevated temperature, a spinal tap in a 6-month old child is a routine. 

In my opinion, the failure to perform the spinal tap at that time was a departure from the accepted standards of care. In my opinion, that most likely would have shown the presence of bacterial germs. 

Prescribing the antibiotic, Bactrim, as well as injecting her with the antibiotic, ceftriaxone, would only serve to slow down the growth of germs and delay the onset of the full expression of the symptoms that she had.

The Emergency Room Physician obviously was concerned about a potential life threatening infection (bacteremia) wherein he ordered and had obtained a culture of the blood for germs. I do not understand why, under all these circumstances, he did not perform a spinal tap or have the patient seen by a Pediatrician, especially when the urinalysis was not consistent with his diagnosis.

On April 25, the blood count showed that the white count was significantly elevated to 24,000, and the differential smear, distinguishing the type of white cells based on their staining characteristics, showed 75 segmented forms, consistent with bacterial infection. The decrease in carbon dioxide (bicarbonate) in the blood shows a trend toward an acid buildup condition, consistent with serious infection. 

The urinalysis obtained on April 25, for the bacteriology examination for germs, showed that the final culture results, available on April 27, showed "no growth." The two Physicians listed on that form are Dr. #2, whose name resembles the signature that was illegible on the Emergency Room record, and Dr. #1. In addition, the blood culture sample obtained on April 25, had a final result, on April 28, as Streptococcus pneumoniae, a specific type of germ. This record says, "results called on 4/26 at 0200 by lab to ER." Therefore, this blood specimen that was drawn on April 25, at 11:12 a.m., had a positive finding documented and called to the Emergency Room 15 hours later. 

This is a life threatening emergency, and their failure to act upon this, in my opinion, is a departure from the standards of care. The Hospital #1 and their Emergency Room, and any personnel involved with this blood specimen, departed from the accepted standards of care. Again, both Physicians' names noted above are on this document. They have a duty to follow up and, in my opinion, they were negligent in the failure to follow up on this seriously abnormal bacteriology blood test, consistent with a life threatening condition.

In my opinion, the patient should have been contacted, through her grandparents, and immediately hospitalized with appropriate cultures of the spinal fluid and other parts of her body obtained, and the patient should have been started on intensive intravenous antibiotic therapy. In my opinion, therapy at that time for the positive blood culture would have prevented the patient developing the severe meningitis that resulted in her seizures, hospitalization, a seizure disorder, and hearing loss.

The patient was next seen by Dr. #3, an associate of Dr. #1. By that time, the emergency results should have been made available to those Doctors, and the record dictated by Dr. #3 says, "the child was seen in Hospital #1 where blood cultures and urine showed probable urinary tract infection. She was put on Bactrim (a sulfa-type antibiotic)." This, of course, was not true. If that Physician would have seen the Emergency Room record which should have been supplied, that Physician should have recognized that the urinalysis was not consistent with a urinary tract infection. Furthermore, by that time, the blood culture results were available and should have been made known to Dr. #3. His office staff should have obtained that information from the hospital, and this patient should have been immediately hospitalized as I described above.

At that time, the ears did not show infection and "the neck is supple." A supple, or soft mobile neck is evidence against acute meningitis, but in a 6-month old child, that may not always be positive at that time. His assessment was "viral gastroenteritis, rule out urinary tract infection." 

As I mentioned, a urinary tract infection was already ruled out, and a differential smear of the white blood count, that was markedly elevated to over 24,000, was not consistent with a viral pattern, but was consistent with a bacterial infection with an elevation of the segmented forms. This Physician continued the antibiotic, Bactrim.

The patient was next seen on April 30, this time by Dr. #4 another associate. He said, "the child is listless." He noted the temperature for six days; noted the patient had received antibiotics and had various studies done, including blood work; and noted the child was not in acute distress and that the neck was "supple." The anterior fontanel, the soft spot on the skull, was soft. This is evidence against overwhelming meningitis with swelling that subsequently resulted. His conclusion was "rhinitis (inflamed nose)/fever of undetermined origin." A complete blood count (CBC) was ordered and the father was going to call that afternoon for the results. 

This study showed the white blood count was more than 25,000, but the band forms, the immature white cells that pour out of the bone marrow in response to overwhelming bacterial infection, were 47%. This is grossly elevated, and the segmented neutrophils were also elevated. This degree of band forms is consistent with a life threatening bacterial infection, and Dr. #4 has his name on the form. Why did he not follow up that day on the results? The father was going to call that afternoon for the results, shouldn't the Physician have seen it first?

I want to point out that the culture and sensitivity on the blood that showed the presence of the Streptococcus pneumoniae germ was resistant to the Bactrim (triameth/sulfa). It was also resistant to the antibiotic, cefazolin, but this patient received a different injectable antibiotic of a similar class, ceftizoxime (Cefizox). The laboratory did not test for that antibiotic, and there was a probability that it was sensitive to that antibiotic. Thus, the injection the child got in the Emergency Room might have been an appropriate antibiotic for therapy, although it was only a one-shot injection. It could help suppress the growth of germs, but obviously did not cure the infection. 

There was a clear opportunity, after 2:00 in the morning, when the positive blood culture was called to the Emergency Room, for someone to intercede, contact the grandparents or mother, and arrange for immediate reexamination and treatment of this patient with a potential life threatening illness. In my opinion, the failure to do so, not only was negligent, but prevented proper therapy that would have treated or prevented the bacterial meningitis and its consequences. 

The patient was then seen on May 1, at the same by Dr. #4. The patient had been on the antibiotic Bactrim for five or six days, still was irritable, and was pulling at her ears. Her neck was supple on examination, and the left tympanic membrane (eardrum) appeared injected (red and inflamed). The Physician diagnosed left otitis media (left ear infection), stopped the antibiotic Septra (Bactrim), and changed the antibiotic to Cefzil. I do not understand why they did not have access to the laboratory tests that had their names on it, as well as the Emergency Room records, since they sent the patient to the Emergency Room for care.

The patient developed seizures and was taken to the Hospital #2. A spinal tap showed the presence of meningitis caused by the streptococcal germ, the patient was placed on appropriate intravenous antibiotics including the antibiotic Vancomycin, and was given appropriate medical attention.

According to the documentation, a CAT scan showed hydrocephalus. The spinal fluid is made within the hollow chambers of the brain called the ventricles, and it passes through a series of narrow passageways to exit from the central portion of the brain and reach the outer surface of the spinal cord, where it is absorbed. The infection caused a blockage of these narrow passageways and the fluid built up within the brain, squashing the brain against the skull, the condition which is called hydrocephalus. Because of that, a drainage tube had to be inserted by a needle operation, a ventriculostomy to drain the spinal fluid under pressure, and they also inserted a pressure gauge to measure the elevated intracranial pressure, and this would serve as a guide for therapy. This care was proper.

Apparently, a follow up MRI was negative. The electroencephalogram (brain wave study) was also negative (although the patient was receiving anti-seizure medication at the time). A BAER test was done, and apparently those results showed nerve damage as it relates to hearing. That, in my opinion, would be related to the meningitis.

The patient was in the Hospital from May 2 through May 16, and in my opinion, received proper medical attention during that Hospital stay. 

In my opinion, there was negligence by the doctors named, as well as the Emergency Room at the Hospital and their treating Physicians. This patient obviously did not have a urinary tract infection based upon the negative leukocyte esterase test and the lack of bacteria or significant amount of pus cells in the urine. That culture was negative. The blood culture was positive for lifethreatening infection by germs, and this was apparently not communicated to anyone who followed up, which left the patient untreated and in a serious zone of danger. Those germs did enter the spinal fluid, causing meningitis. Possibly, they originated at that site, but in any event, it went untreated, or received inadequate antibiotic therapy, and thus partial suppression therapy, despite the laboratory results they had, including the markedly elevated white blood count with the gross elevation of the band forms that I described above. This is called a "shift to the left."

The Physicians will contend that the patient looked well, according to their office records, and her neck was supple. But this is a 6-month old baby, who was not receiving proper medical care. Even if they believed that the blood culture was a contaminated study, the white blood count with a marked elevation of the white cells and a gross shift to the left with 47% band forms (some of the highest I have ever seen on a smear), was a red flag that was not heeded. They were treating her for a urinary tract infection that did not exist, according to all the laboratory tests.

The differential smear on May 1, showed 81% segmented neutrophils, and only 6% band forms. The previous day, the differential was performed by the technologist. This one on May 1 may only have been the automated, computer-generated analysis. However, even on that study, there was "1+ toxic granulation," where as on April 30, there was 2+ toxic granulation and Dohle bodies. These are seen with overwhelming bacterial infection.

Is this child still having seizures? Is she still on anti-seizure medication? Have follow up hearing tests been performed since the last ones noted in the record? The developmental analysis shows there was "mildly delayed motor skills." She has "mild hypotonicity and muscle weakness, especially of the upper trunk and upper extremities." Perhaps she has had more brain damage than just hearing loss. Has this been followed up by any evaluations by a Pediatric Neurologist? The examination I am referring to occurred nine months ago. Have there been any recent MRI studies of the brain to be sure that there has been complete resolution of the hydrocephalus?

I would suggest that we obtain the services of Board Certified Experts in the fields of Emergency Medicine and Pediatrics, to discuss the negligence in this case. I would also suggest that we obtain Board Certified Experts in the field of Infectious Disease, to add their expertise as to how proper therapy at the correct time would have prevented the progression of the infection. In addition, you may also want us to supply an Expert in Pediatric Neurology to discuss all aspects of negligence, causation, and damages. All these Board Certified Experts are available through our independent consulting staff, pursuant to our current Fee Schedule.

Thank you for allowing our organization to assist you with this important case.

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Gunshot wound to the heart with collapsed lung and pericardial tamponade (clots squeezing the heart like a vice), emergency open chest surgery and failure to suture the two holes in the heart.

At age 21, the patient, under the influence of alcohol, dropped his gun while getting into a car. It went off, penetrating his chest to the right side of his sternum (breastbone). His friends immediately drove him to the emergency room of Hospital #1. They carried him inside and, after taking off his clothes (standard procedure), "they started pinching his chest, and calling his name, he didn't respond."

He arrived at 0018. They ventilated him with a hand-bag ventilator and mask unit. A bladder (Foley) catheter was inserted. His blood pressure was good at 154/99. Intravenous lines were attempted in the neck area (subclavian catheter insertion), but were initially unsuccessful. At 0024 he had an endotracheal tube inserted into his windpipe (intubation) and the oxygen blood saturation was acceptable at 93% (which was taken when he was still on the mask / bag unit).

At 0029 the oxygen saturation dropped into a barely acceptable but dangerous range at 73%. This is consistent with a collapsed lung and further lung compression by air trapped between the lung and the inside of his rib cage (tension pneumothorax).

At 0029 his blood pressure was 130/110 and pulse rose from 49 to 103. This narrowing of the pulse pressure from 154/99 to 130/110 is consistent with pericardial tamponade (clots from a hole in the heart trapped between the heart and the pericardial (heart) sac, constricting it like a vise. That was ominous.

At 0030 they correctly gave him the drug Narcan for a suspected narcotic overdose, since he was non-responsive on arrival with a good blood pressure.

The emergency portable chest x-ray that was ordered at 0030 was taken at 0031. Blood was drawn for testing. A second dose of Narcan was given at 0033, acceptable care.

By 0034 blood and normal saline (salt-water intravenous fluids) were being rapidly administered.

At 0035 Dr. #1, the Emergency Room Physician, inserted a #14 size tube into the right chest to relieve the air pressure from a suspected tension pneumothorax which can cause shock and decreased blood oxygen that they found. That was good care. It would not drain blood, but would release the air pressure, if present.

At 0035 there was no blood pressure and no palpable (by feel) pulse. CPR (cardiopulmonary resuscitation) was started at 0037. At 0037 the chest x-ray showed a gunshot wound (gsw) to his heart. His heart rate was 51 at 0039. CPR continued. At 0040 a larger chest tube was inserted into his right chest by Dr. #1, to drain blood.

At 0047 Dr. #1 used a scalpel to cut open his right chest (thoracotomy) and found a large amount of clotted blood. Why did he wait those extra minutes after the chest x-ray result was known, and even after he inserted the chest tube? They increased the normal saline infusion amount at 0049, epinephrine (adrenaline) was given to try to stimulate his heart to pump harder, to raise his blood pressure at 0051 and by 0055 Dr. #1 was suturing the hole in the "right ventricle" chamber of his heart. The right ventricle pumps all the venous unoxygenated blood under moderate pressure into the pulmonary artery and lungs. This was "completed" at 0058 (excellent time), and Dr. #2 arrived to evaluate the patient.

The gunshot wound was fatal since, with all their excellent efforts, they were not able to resuscitate him, even with manual (hands on the heart) compression. At 0100 they stopped CPR, no pulse was noted at 0101, and he was pronounced dead at 0105.

The autopsy revealed that this 5'8", 122-pound young man sustained a 1.0 x 1.5 centimeter (one inch = 2.54 centimeters) entrance wound to his right chest and: "There is a wound in the anterior wall of the right ventricle 1.5 centimeters. The pericardial sac adjacent to the exit wound contains multiple sutures and there is hemorrhage in the left lung." Also: "The pericardial sac contains approximately 200 cc (7 ounces) of partially clotted blood."

It also said: "The entrance and exit wounds are in the right ventricle. The entrance wound is in the anterolateral (top / side) portion and the exit wound is in the anterosuperior (upper top surface) portionnear the pulmonic valve. The left ventricle (main pumping chamber of the heart which pumps the oxygenated blood received from the lungs, to the whole body) is unremarkable. There are no other valvular or muscular abnormalities." Other than some hemorrhage in the left lung: "There is hemorrhage and multiple sutures in the hilar area (where the pulmonary artery brings blood from the right ventricle to the lung to become oxygenated) where there are small wounds," everything else was normal. Apparently the bullet broke some cartilage or bone on the way into the chest, spraying fragments at high velocity, which pierced this flesh, or cut through the hilar area before it pierced his heart. The bullet was recovered and "given by Dr. #1 to the police detective."

When there was evidence of pericardial tamponade, most physicians would have attempted to do a pericardiocentesis (using a needle and syringe to withdraw some of the non-clotted blood within thepericardial (heart) sac). However, with that large hole in the right ventricle, it would have not been successful and it could not remove the clots (like jello) that serve to compress the heart like a vise, and will eventually cause death.

When he opened his chest, he thought he was suturing the hole in his heart, and failed to do so, and failed to recognize that he was suturing the pericardial sac, which assured the pericardial tamponade (which contained 200 cc [cubic centimeters] of clots at autopsy), to be a fatal blow.

With the holes in the hilar area, and the hole in the right ventricle, the area would be flooded with blood and, unless he was an experienced chest (thoracic) surgeon or cardio-vascular surgeon, or a general surgeon with some of that training, the average emergency room physician, although doing all he could, would not possess that higher sub-specialty training.If you are going to proceed with this case, it is first essential to determine all of the training of Dr. #1, particularly any he may have had in general or thoracic surgery and in hands-on training and experience in treating gunshot and stab wounds to the heart. I had treated four in training and one in practice. All but one lived. However, there was assistance by other residents and an emergency room and operating room that was a major trauma center which saw such patients as this one, on an all-too-common basis.

After you discover all that about Dr. #1, and discover the training of Dr. #2, and when he was called, where he was when he got that call to get him there at 0058, I would then suggest these records and that information be reviewed by a Thoracic or Cardio-vascular Surgeon. That Surgeon can give you their opinion if Dr. #1 was negligent in his surgical technique, and what if any difference it made to the death of the patient. Also, that doctor or a neurologist would then have to give you their opinion as towhether, if he would have survived, the degree, if any, of brain damage he would have sustained from 0035 when his pulse was lost, to the time that the thoracic surgeon may opine he would have recovered his blood pressure, and thus brain-sustaining oxygen flow.

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Head injury after a seizure or beating with lethargy assumed to be from the seizure, no CT scan, and sent home with intra-cerebral hemorrhage causing brain death.

When a patient is seen in an Emergency Room and they have been found at the accident lethargic and still are lethargic, their head must be examined to rule out head injury. If they have a seizure history, it cannot be assured that persistent lethargy is the "normal" result of a seizure (post ictal state). If there is any question, a CT scan of the head (brain) is indicated to rule out hemorrhage (bleeding) into the brain.

At age 35, before 12:15 a.m. on 5/19, he was "nonresponsive and found laying on ground." He responded to an amonia inhaler and they wrote "ETOH (alcohol)?" It was on his breath, but they did not test the alcohol blood level in the Hospital #1 emergency room.

At 0030, he was examined by the Emergency Room physician whose signature is illegible but whose name on the laboratory results is Dr. #1. He noted a "one centimeter (2/5 inch) mucosal abrasion of upper lip," but did not note any skull examination. That failure is a departure from the standards of care. He noted that he patient was "drowsy" but "responds to pain stimuli." He was not alert.

The doctor's final diagnosis was: "1) Breakthrough seizure secondary to subtherapeutic phenobarbital." The blood level of that antiseizure medication was 10.6 with the treatment range of 15-40. He also concluded: "2) ETOH (alcohol) intoxication," but had no blood level test.

At 0040, he ordered the patient to receive 5 milligrams of Valium, intravenously. That can prevent further seizures, but was given five minutes before the seizure medication blood tests were even ordered. And Valium can cause drowsiness, as can brain injury. A second 5-milligram dose of Valium was given at 0400, but no reason noted.

At 0200, he was "waking up - trying to climb out of stretcher." At 0245: "Dozing, arouses and tries to get off stretcher. Strong smell ETOH (alcohol). Waiting until more awake before discharging him to home."

At 0300: "Vomited up about 200 cc (7 ounces) clear ETOH smelling liquid." Vomiting is also consistent with brain injury.

And at 0550, he was "Discharged home with family per wheelchair. Instructions given." At that time, his pulse had been abnormally slow (51, 55) at 0415 and 0600, which is seen with brain injury.

How awake was he? Obtain witness affidavits.

He was to: "Return to Emergency Department if problem worsens." He also was to take his antiseizure medication and: "Increase phenobarbital to 60 milligram pills daily." The head injury box on that same page was NOT checked off.

When he was re-examined by that same doctor at 5 a.m. again, there was no head examination. And he noted: "Feels drowsy - probably secondary to Valium intravenous."

Since he did not examine his head, and gave him a medication that has the same side effect as an injured brain, in my opinion, he had a higher duty to obtain a CT scan of the brain. Even without the two doses of Valium, he had a duty to obtain a CT scan.

What time was he found in the alley? What injuries were visible? The medical history is negligently deficient. The longer the interval between finding him and the initial examination, the greater the concern there should be for head injury as the cause of his initial comatose state. Furthermore, if as this doctor noted, he has concern for "ETOH intoxication" as his "Final Diagnosis" why didn't he obtain a blood level test for alcohol? Alcohol intoxication can cause drowsiness, but can also cause a fall and head injury, as can a "breakthrough seizure."

In my opinion, this Emergency Room Doctor departed from the accepted standards of care in his 1) inadequate history available from his family; 2) failure to examine his skull for signs of injury and recording it in the medical records; 3) use of Valium twice without finding a cause of his initial coma and subsequent drowsiness that responded to painful stimuli; and 4) failure to order a CT scan.

In my opinion, that CT scan would have been positive for intracerebral hemorrhage. A Neurosurgeon should then have been called in for an immediate consultation to further evaluate and treat this patient. Most likely, he would have had surgery to drain the blood clots before they caused irreversible coma.

How did the patient progress at home, hour by hour?

Nine and a half hours later (on 5/20 at 1430: 2:30 p.m.), he was again taken to that same emergency room. His pulse was 53. He was very lethargic. His wife said: "He just wants to sleep all the time." Obviously, the Valium had worn off. He was given his phenobarbital. At 60 milligrams in a patient who had taken it chronically, it should not cause lethargy. This doctor noted that the patient (on the previous night) was found outside in the alley "down with bleeding." Bleeding from where?

Although he was awake at 1430, he was "mumbling" and gave "no cohesive response to any questions." An urgent CT scan was performed that showed blood in the skull, on the surface of the brain and in the left frontal lobe. It pushed against the brain and shifted it one centimeter (2/5 inch) from left to right. There also was "diffuse cerebral edema" (brain swelling).

He rapidly went into a deep coma and had a dilated left pupil (from the swollen brain squashing the nerve for pupil control against the skull). At 1515, he received the potent steroid, Decadron, and at 1530 he received the power diuretic drug, Mannitol, to shrink the brain to try to save his life, while the Decadron would help to fight the cerebral edema.

All this is good care, but should have been given hours before when they had the best chance for preventing his irreversible coma. The swollen brain from hemorrhage and injury will compress their blood supply to the brain (just as it squashed the nerve to the left and then also the right pupil) causing brain death.

He was air flighted to the Hospital #2, leaving at 1735 with his airway protected by an endotracheal tube (for secure ventilation). It was initially attempted to be inserted via his nose but had to be put in place orally. That temporary nose bleeding was not from poor care.

He arrived in a deep coma. It was felt that he had irreversible brain damage. The wife agreed to a Do Not Resuscitate order. An "apnea test" was done temporarily off the ventilator, and he would not effectively breathe. That study, plus all the tests for deep coma resulted in the removal of the ventilator and his death. His mother refused organ donations and that was honored by his wife.

Because of the concern for his injury secondary to a beating, an autopsy was to be done. I have not seen that examination and the compete report should be obtained. Obtain copies of photographs of his brain.

Also obtain a compete copy of the 5/20 CT scan of the brain. If they still have the original computer tapes, they can general another "original." Do not send the only original copy.

In my opinion, the first Emergency Room Physician, who may be Dr. #1, any Emergency Room corporation, and the Hospital #1 were negligent for all the reasons stated above, and that negligence was the proximate cause of an increased risk of his death.

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The defense would contend that with any closed head injury, there can be bleeding that is not always amenable to surgery and anti-edema therapy. But the failure to diagnose and timely treat markedly increased that risk.

The defense will contend that he would have been left with profound brain damage. However, the major hemorrhage into his brain involved only his left frontal lobe, which can be sacrificed with possibly a more blunted affect (one-half of a prefrontal lobotomy).

The defense will argue his sociological factors: Crack cocaine use (abuse) confirmed by a positive urine test, which also was positive for marijuana. And his alcohol use / abuse questions. Did he have any positive work and drug rehabilitation history?

In this case, I would suggest that after you obtain the missing autopsy report and copies of the brain CT scan and answers to the questions above, that you authorize us to have all these records reviewed by Experts in Emergency Room Medicine and Neurosurgery. Possibly Experts in Neurology and Rehabilitation Medicine could address any residual injury if he would have lived. And with all the medical and sociological records and information, an Expert in Drug Addiction Treatment could address his potential for rehabilitation.

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Elderly patient with severe vomiting forced fed x-ray dye, vomits and chokes in a CT scanner, and delayed and improper resuscitation with coma, and then perforated stomach and surgery from medication errors, and followed by death.

This 73-year-old woman weighing 176 pounds developed abdominal pain and persisting vomiting. The Primary Care Physician (PCP) "gave her" a suppository for nausea on March 10. Obtain that doctor's records. Did he or she examine this patient? On what basis was the anti?nausea medication prescribed? What warnings and follow-up instructions were given to her? Who was present?

On March 12 she came to the Hospital # 1 because of persisting vomiting. She had been taking the steroid pill, prednisone. What dose, for how long and for what reason? Steroids can cause stomach ulcers and perforation. Perhaps its prescription was not indicated. Was she advised of all the risks from taking steroid drugs?

Acute steroid withdrawal can cause a form of shock. She was not in shock in the Emergency Room on March 12 or thereafter because she received intravenous steroids.

Her abdomen was tender and she said she felt better after vomiting. What color was her vomitus? It is not recorded in the record, and the color is very important to aid in a diagnosis. If it is green, it means it contains bile from her liver, which empties into the small intestine (duodenum), and therefore, any blockage (obstruction) is below that point. If it is clear, or very light yellow, it usually means that the stomach is obstructed (above [upstream of] the bile duct entrance).

The Emergency Room Physician #1, DO (Doctor of Osteopathy: like a Medical Doctor and held to that same standard of care), noted she had frequent vomiting and ordered the standard abdominal x-rays (survey) with her lying and standing. It did not reveal small bowel obstruction findings (distended loops of small intestine and air fluid levels: Like looking at a glass of water from the side). Therefore, most likely there was stomach outlet obstruction. He ordered the abdominal CT scan with contrast. The Radiology Department has a standard printed order form that instructs the nurse to put 35 cc (one ounce) in 1000 cc (one quart) of tap water "for adults" and to have them drink it all one hour prior to the CT scan. That volume will fill the stomach and most of it would flow into the 25 feet of small intestines, serving as a radiopaque (x-ray blocking) contrast dye.

By 1235, she drank 400 cc (13 ounces) and was reminded two times to drink it all. "Patient stated 'this will make me sick' and will cause her to have 'problems breathing.' Patient instructed to continue drinking prep. Husband at bedside."

At 1250, "Reminded patient needs to be drank (sic) in ? hour or NGT (Naso-Gastric [stomach suction] tube) will be tried."

At 1315: "NGT reinserted #16 (size of a #2 pencil) via (L) nostril. 200 cc (7 ounces) prep injected." Previously, at 1150, it had been inserted after two attempts. Three minutes later she pulled it out. It again was re-inserted and "while in X-ray (Department) NGT fell out."

At 1557 (obvious error in time sequence), it was noted she was "getting breathing treatment, patient c/o (complained of) not able to breathe." She was sat upright.

At 1305, the patient was called to go to the CT scan room.

She was put into the CT scanner, and the abdominal scans were done. At that moment she began to vomit and the naso-gastric tube was still in her stomach, based on the CT scan. That tube increases the risk of regurgitation, as well as increases the risk of choking because of its presence in the back of her throat.

The CT scan showed stomach outflow (to the intestines direction) obstruction by a volvulus of the stomach (total twisting) or a pyloric ulcer (at the opening between the stomach and the duodenum: First part of the small intestine) with edema (swelling).

She developed a cardio-respiratory arrest cased by a large amount of vomitus in her throat and her (or their) inability to turn to her side while in the CT scanner. The Emergency Room physician, Dr. #2, saw her urgently at about 1500. He noted: "She then complained that she was having difficulty breathing (for how long?) and promptly started vomiting. The patient had copious amounts of vomiting. She was removed (after how much time delay?) from the CT cradle and placed in the lateral (side) recumbent position. At that time she was noted to be in respiratory arrest."

In his note he said, "CODE was called and at that time of my arrival the patient was found supine (on her back) on the examination table with copious amounts of vomitus around her mouth. She was being ventilated with a bag-valve mask. On my arrival, no pulses were detected…suction device was (then and after how much delay?) hooked up and her oropharynx (mouth and throat) was suctioned…and the patient continued to be ventilated with a bag-valve mask."

Therefore, it appears that she may not have been timely removed from the restrictive CT scanner, and probably had the mask applied over her face with a mouth and throat full of vomit, which would force it into her lungs, impairing ventilation and increasing the risk for pneumonia, which occurred. The delay in suctioning increased the risk of adequate and on-time oxygenation causing difficulty in full resuscitation and brain damage (coma from anoxic encephalopathy).

Since the abdominal x-ray did not show small bowel (intestinal) obstruction changes and she was on steroids, the probability of an obstructing stomach ulcer was high. If the vomitus was not bile (dark green) colored, then it would be almost certainty caused by the ulcer. Treatment would be to decompress the stomach with a naso-gastric tube, give her intravenous (IV) fluids and a very potent anti-acid IV medication, such as Pepcid. This should resolve over a few days.

In my opinion, their initial evaluation was negligent as noted, and led to an unnecessary CT scan with one quart (1000 cc) of Gastrografin containing tap water force-fed to a patient who had pulled out that tube three times before and refused to swallow any more than 400 cc.

This would appear to be assault and battery, as well as negligence.

Then there may have been negligent delays in removing her from the CT scanner. There was negligence in using mask-bag ventilation without first suctioning her throat. Also, when did they empty her stomach of any residual via the present NG tube?

When she contacted her Primary Care Physician with vomiting, did that doctor who prescribed the steroid prednisone, (or should have known of her use of that drug), examine her or just issue and anti-emetic (anti-nausea/vomiting) suppository? Obtain all those records. Perhaps the steroids were also negligently prescribed, and they significantly increased the risk of this acute stomach ulcer developing.

Finally, when she was admitted to the hospital by Dr. #2 at 1130 a.m., he ordered Pepcid 40 mg in 50 cc fluid (2 ounces) to go IV at 11 cc/hour. After the arrest she was admitted to the ICU at 1630 and neither he nor anyone (including Dr. #3) re-ordered it to be given. It is standard practice to re-write all patient medication and therapy orders upon transfer to the ICU. That negligent failure to re-write the Pepcid by the Physicians and the negligent failure of the Nurses to inquire regarding the Pepcid order, increased the risk of that ulcer perforating by early a.m. on March 13. This was confirmed by the abdominal x-ray showing pneumoperitoneum (free air in the abdomen from a perforation) and the perforated stomach was found at the needed (to save her life) surgery on March 14 by Dr. #2. Pepcid was first given to her on March 15.

All her other care after her coma appears proper. She had profound and irreversible brain damage and died after the ventilator was discontinued on March 18. No autopsy was done.

In my opinion, the Emergency Room Physician, Dr. #1, any corporation that employed him, the Emergency Room Nurse, the hospital, the Radiologist in charge of the CT scanner at the time, his partnership, the Radiology Department, as well as the radiology technician(s) involved with her CT scan, and the Hospital #1 are all negligent for the reasons stated above as it relates to her coma and death. Dr. #2, the Intensive Care Physician, and the ICU Nurses were negligent for not continuing the anti-acid mediation while she was receiving potent IV steroids and just had that neurologically stressful "event," which is known to also increase the risk of stress ulcers. That increased the risk of her stomach ulcer perforation, causing the need for the stomach surgery. However, she was in a very deep coma and did not respond to painful stimuli, so the damages were its cost and the emotional effect on her family.

Furthermore, the Primary Care Physician may be negligent if the steroids she took (prednisone at an unknown dose and for an unknown length of time and diagnosis) was not medically necessary and if she was not informed of the risks. This would also depend on how she obtained that suppository for nausea and vomiting. The Emergency Room records note that her family Physician was Dr. #4.

I would suggest you obtain those missing records and information and you authorize us to have all these records evaluated by Experts in Emergency Room Medicine, Radiology and Family Practice or Internal Medicine (depending on the specialty of her Physician) and a Nurse with ER experience.

If you want to pursue the stomach perforation issue in the hospital, then I would suggest a General Surgeon and ICU Nurse Expert.

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AIDS Patient comes to Emergency Room with pneumonia and needs a ventilator. He gets steroids, gets worse and dies.

When a patient is HIV positive and has AIDS (Acquired Immuno-Deficiency Syndrome), his immune system is very impaired. This patient is very susceptible to infections, including pneumonia.

If a patient has asthma (a spasm of the brachial tubes), then in addition to bronchial dilator medications and antibiotics (if he has an infection), the use of steroid medications may be necessary to help overcome the allergic nature of the cause of the bronchial tube spasm. The lungs will have high-pitched wheezes, not rhonchi (wet, congested) breath sounds.

This patient, at age 62, was HIV positive and developed shortness of breath and pneumonia. He had "rhonchi" and no wheezing. There are no x-ray reports in the medical records, and they should be obtained.

In the Emergency Room, he was evaluated and they noted he had been to other hospitals emergency rooms recently and received antibiotics. Their records should be obtained.

He received antibiotic therapy for his pneumonia. The usual standard of care is to obtain a sputum (deep cough) specimen for laboratory testing (culture and sensitivity) to determine which germs are present, and the best antibiotics to kill them. I do not find that in the records, and if it was not done, is a departure from the proper standards of care.

Upon arrival and for the entire stay (6/24-7/1), he received potent steroid medication by intravenous injection (30-60 milligrams of Solu-Medrol every 6-12 hours). He had no wheezing or evidence of bronchial spasm. In my opinion, this worsened his already damaged immune system's ability to combat any infection.

On admission, his arterial blood oxygen level was very poor and required an oxygen mask. I will discuss this issue in some detail. The red blood cell pigment is called hemoglobin. It holds oxygen like a sponge holds water. However, its grip is not linear. It follows an "S" shaped curve. Room air is 21% oxygen. With normal lungs, the pressure of oxygen in the blood is 95-99 (PO2 ,also called TORR). The saturation of the hemoglobin is normally close to 100%. With lung disease (including pneumonia), less oxygen enters the blood, but the hemoglobin still is highly saturated. With an oxygen pressure of 50-60, the hemoglobin is usually 85% saturated. But that is at the beginning of the sharp downslope of the "S" shape curve. With a little further drop off of the arterial blood oxygen pressure (PO2), the saturation falls dramatically, the patient turns blue and will die.

In his case, on 6/23 at 3:28 p.m., his PO2 was 74.2 and his oxygen (O2) saturation was 86.5%. On 6/30, with an oxygen mask giving him 50% oxygen to breathe (versus 21% on room air), his PO2 (oxygen pressure in his arterial blood) was only 50.8 and his oxygen saturation was 90%. His condition worsened late that night. He was not intubated (tube put into his windpipe (trachea) and a ventilator was not used to force oxygen into his lungs to increase the oxygen in his blood). The mask would not work with his lungs failing from pneumonia.

His blood count also worsened, consistent with severe infection. The white blood count (WBC) ws normal on 6/23 at 5100 and had risen to 12,000 on 6/30. But the differential smear changed (shift to the left), consistent with severe infection. He became very anemic (less red blood cells and hemoglobin to carry any oxygen to his body's cells), the platelet count (clotting particles made in his bone marrow) dropped severely (thrombocytopenia) and he would bleed. All this hospital stay he received high doses of the steroid drug Solu-Medrol, as I noted.

He required this ventilation mask, but then on 6/30, he required the intubation and ventilator. However, on 6/30, at 8 p.m., when he was still alert and conscious, he signed a consent form for "no intubation." The hospital personnel considered this the same as a Do Not Resuscitate (DNR) order, but it is not quite the same. As few hours later, they watched him die.

In my opinion, the abuse of steroids allowed the lung infection (pneumonia) to progress, which ended his damaged life. Without the steroids and with the correct antibiotics and pulmonary care, he had a better chance to live.

I suggest that you obtain the missing records (x-ray reports and any culture and sensitivity bacterial reports). I also suggest that you obtain good copies of the chest x-rays and the previous emergency room records, plus all documentation as to his HIV and AIDS status. Then authorize us to have all these records evaluated by one of our Board Certified Emergency Room Experts and an Infectious Disease Expert for their opinions as to the care at this hospital and by those Physicians, as well as try to determine his AIDS status and potential longevity.

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Diabetic foot infection mistreated resulting in gas gangrene and leg amputation.

The patient was 56 years old at the time he presented to the Hospital on August 4 complaining of left foot swelling that evolved over four to five days with a painful blister on top of his foot. At the time of this presentation to the Emergency Ward, it was well established that the patient had been a noninsulin-dependent diabetic for decades. The history was also obtained that the blister had been present for more than a month and had become increasingly painful to the point where he was unable to bear weight on his left foot. The patient denied preceding trauma.

The medical records are clear that the patient underwent blister drainage following a supposedly normal x-ray of the left foot. The blister drainage procedure was performed by Dr. #1 and revealed 1-2 cc of bloody fluid in the absence of pus. Of note, this fluid was not submitted for culture or gram stain analysis, which would have been the appropriate standard of care to perform in a diabetic when infection has not been excluded. A gram stain is a rapid microscopic analysis that can be invaluable at pinpointing infection and defining the bacterial type of infection involved so that appropriate antibiotic therapy can be begun.

The patient, although afebrile (without fever), did not have routine diabetic studies performed, nor was a CBC, a basic blood test to help exclude infection, obtained.

It can be stated, within a reasonable degree of medical certainty, that the standard of care when a diabetic patient presents with an unexplained, painful foot blister, is to assume the blister is infected until proven otherwise. Although the role for drainage of such blisters is controversial, once the blister is drained, it is imperative that the fluid be analyzed to rule out infection. In fact, the presence of bloody fluid in the absence of pus is typical of infection with bacteria of a less pyrogenic (pus-producing) nature. These bacteria are not uncommon in diabetics.

In addition, it is well established that diabetics can have smoldering, low-grade infections and they often have atypical presentations of these infections.

It is also well established that diabetic foot infections are a major cause of potential limb loss as well as serious complications, especially if undertreated or underappreciated.

Even if infection was not strongly suspected prior to this drainage procedure, it should have been quite apparent to his Emergency Room caretakers that any drainage procedure would predispose this diabetic to further risk of infection due to the introduction of soft-tissue skin breaks. No systemic antibiotic therapy was prescribed for him before, during or after this drainage procedure and no antibiotic or antiseptic topical preparations were applied to the foot wound. It is also unclear as to what type of dressing was applied in this setting.

The patient was discharged from the Emergency Room with a diagnosis of musculoskeletal foot pain. He was prescribed a medication known as indomethacin, which is a nonsteroidal anti-inflammatory agent that can mask fever as well as the classic inflammatory signs and symptoms of infection if and when such infections subsequently develop.

It is also apparent from the Emergency Ward records that an inadequate attempt was made at patient education in terms of what signs or symptoms needed to be watched for. The patient was given, for example, no instructions in terms of what to do should redness or streaking of the foot or increasing pain develop. In short, the discharge instructions that this patient was given were inadequate. His entire Emergency Room work-up fell far short of the standard of care for handling a diabetic foot wound when infection has not been adequately excluded. Similarly, there was not even an attempt made to gauge the effect that this foot process had on the patient's diabetic state since no blood glucose monitoring was performed on this Emergency Ward visit.

Additionally, he was given instructions to seek follow-up with his Primary Care Physician, Dr. #2, on August 17, a nearly two-week delay. This is far longer than is the recommended time frame for follow-up following an incision and drainage procedure from which infection had not been adequately excluded.

Also, the Emergency Ward Physician's preliminary radiographic impression of a normal foot film was erroneous. The official reading of this report was consistent with a neuropathic joint or trauma, which we know this patient did not sustain. In addition, subchondral erosions that were seen within the joint of the cuboid and fourth metatarsal joints could well have been consistent with osteomyelitis or even septic arthritis, two very serious conditions for a diabetic to experience. The official radiographic interpretation by Dr. #3 was made on August 5 and reverified on August 6 such that the Emergency Ward physician, Dr. #1, had ample time to intervene to have the patient return for further Emergency Ward evaluation.

On August 17, the patient, while going to his follow-up appointment, sustained a fainting episode and was admitted to the hospital, at which time the diagnosis of gas gangrene was made and he promptly underwent a guillotine amputation at the below-the-knee level.

On the date of this hospitalization at the Hospital, the wound size had markedly increased from 1 x 1 cm to 4 x 8 cm, and was actually draining pus and gas. This condition, that of a wet gas gangrene with cellulitis, required urgent operative intervention. I have no qualms with the decision to have the patient undergo a guillotine below-the-knee amputation procedure. He underwent this procedure on August 24, which, although somewhat delayed, nonetheless needed to be done, and this procedure was appropriate.

Although I also have some reservations regarding the use of the antibiotic ampicillin sulbactam, this was not a medically treatable condition and gas gangrene is surgically managed with the choice of antibiotics being less important than the surgical aggressiveness required.

It should also be noted that during this course of hospitalization, he was noted to have kidney dysfunction which was most likely secondary to the combined insults of indomethacin as well as untreated soft-tissue sepsis and a diabetic state.

The condition of gas gangrene is an aggressive diabetic soft-tissue emergency that frequently leads to multisystem failure and a host of other complications, as was seen here, including kidney and cardiac disturbances.

In summary, the Emergency Ward treatment that he received by Dr. #1 on August 4, exhibited numerous deviations from the existing standards of care. These deviations have already been alluded to and include the lack of proper consideration of infection in a diabetic without trauma and with a relatively long-standing foot blister. Other deviations from the standards of care include the incision and drainage of this blister without obtaining proper cultures, gram stain and lab studies, such as a white blood count and kidney function analysis and the incorrect interpretation of the left foot x-ray films. Additionally, Dr. #1 had the opportunity, once the offical x-ray report was finalized, to intervene and get the patient back for an early re-evaluation, but failed to do so. The discharge plan for this patient, including the patient's information regarding what to look for in terms of complications, was insufficient and the follow-up interval of nearly 14 days was overly long by more than a week.

Although diabetics are predisposed to complications such as gas gangrene, the deviations from existing standards of care, were the result of Dr. #1's inadequate Emergency Ward evaluation of this patient, and in my opinion, contributed to the extent that his infection became out of control and resulted in limb loss with a below-the-knee amputation, and subsequent surgical revisions.

Though it could be argued that even under the best of circumstances one cannot guarantee that limb loss might still have occurred, it is more likely than not, in review of these records, that this patient's limb could have been salvaged by earlier and more aggressive consideration and treatment of soft-tissue infection of the left foot. Indeed, documentation by Dr. #1 established that good pulses were present on this foot. This indicated that sufficient vascular supply was available to enable aggressive medical and surgical management to result in limb salvage.

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Head injury in an elderly patient taking an anticoagulant (blood thinner), not given antidote, resulting in brain hemorrhage.

This 90-year-old lady was taking the anticoagulant (blood thinner) Coumadin, fell forward out of her chair and hit her head. Whether or not she was unconscious was unknown.

She was taken to the emergency room of Hospital #1 on 4/12. Her blood pressure was very elevated but returned to a safe but still elevated range without treatment in this known hypertensive patient . She was neurologically intact (with her pre-injury dementia). There was a large bruise on her forehead and bruises on her face. A CT scan without contrast of her head showed no bleeding in her brain, but a large blood clot under her forehead skin. No blood tests were done. No head injury warning sheet instructions were given to her or her family. She was told to see her doctor in one day for follow-up, and I have no information on whether or not that happened.

At home over two weeks she deteriorated, and when she was taken back to that same hospital, she was arousable but with obvious neurological deterioration. The CT scan (without contrast) showed that the scalp blood clot (hematoma) was larger on April 24 than on April 12, and she now had hemorrhage in the back of her brain (occipital lobe) and into the hollow fluid area (ventricle) of her brain.

The blood tests showed a low vitamin B12 level and a dangerously high protime (and INR), three times the safe therapeutic range of the intended anticoagulation effect of Coumadin. They gave her the antidote (vitamin K) and good medical care. The brain blood clot was stable (no change on the CT scan the next day), and not compressing her brain, because of the brain atrophy (loss of brain cells) which was the cause of her dementia.

She was basically comatose, transferred to a nursing home and died on 8/13. No autopsy was done.

There are a number of issues of negligent care. It starts with her abnormally low blood vitamin B12 level. This can cause nerve damage, including spinal cord damage, which can increase her risk of falling. Her physician records need to be obtained and reviewed for that issue.

When she entered the emergency room on 4/12 with an obvious head injury and hematoma, and it was known that she was taking Coumadin, it was a departure from the standards of care (negligence) not to order the protime (PT) and/or INR blood test. Most likely it would have been abnormally high, and the antidote would have needed to be given, and most likely would have prevented or limited the brain hemorrhage. Also, the standard "head injury" warning written instructions needed to be given to her family, and not to do so was also negligent, and allowed her condition to worsen until it had caused more irreversible damage.

When she entered the emergency room on 4/12 with an obvious head injury and hematoma, and it was known that she was taking Coumadin, it was a departure from the standards of care (negligence) not to order the protime (PT) and/or INR blood test. Most likely it would have been abnormally high, and the antidote would have needed to be given, and most likely would have prevented or limited the brain hemorrhage. Also, the standard "head injury" warning written instructions needed to be given to her family, and not to do so was also negligent, and allowed her condition to worsen until it had caused more irreversible damage.

Who ordered and was monitoring her Coumadin? It was ordered for her history of DVT (deep vein thrombophlebitis: clotting in leg veins). Usually it is given for only six months. How long was this medication prescribed, and why? Obtain all those records, because in addition to the issue of proper drug dose regulations, its use at all may be negligent and markedly increased her risk for brain hemorrhage.

The death certificate says she died from coronary artery disease and mentions no other factors. It is incomplete and is in error. Also, blood clots in leg veins (thrombophlebitis) may break loose and enter the heart/lung circuit, causing death. Immobility (bedrest) significantly increases that risk, and she was semi-comatose in bed. The head injury is not mentioned.

The defense will contend that the CT scan showed no bleeding, but it is unclear how many hours elapsed from her head injury until the CT scan was taken. Also, no contrast was used; contrast would be more accurate. Perhaps it was misread by the Radiologist. I would suggest very good copies of the 4/12, 4/24, and 4/25 CT scans be obtained for review by a Radiology Expert. They can make a new "original" from the computer tapes, or a good copy from the standard processing, where you cannot tell then apart from the original when viewed side by side.

The Defense will contend that she was demented and had a poor quality of life. They will also claim, that at age 90, she had very little longer to live (statistically).

To proceed in this case, please supply the missing records and answers to questions. Then authorize us to submit these records to our independent Experts in Emergency Room Medicine, Neurosurgery, Radiology, and the same specialty of her treating Physician.

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Not diagnosed heart attack and developing stroke was claimed.

His wife claims that she arrived at the hospital shortly after 10 o'clock in the morning. I do not have all of the emergency room records, but the dictated report claims that the patient was seen by the clinician at 1700 (5:00 p.m.). I have the second and third pages of the nurse's notes, which are preprinted as "page 2." This shows the first recording of blood pressure was at 1710 and was 226/125, which was significantly elevated. This was treated with a blood pressure lowering medication, Normodyne, at 1830, and the blood pressure dropped down to 195/92, and five minutes later was about the same. It was only moderately elevated at 185/82, which is a reasonably safe range. At about 11 p.m., the patient was admitted in to the hospital, into the surgical intensive care unit. I have not seen those nurse's notes, and the first few days of nurse's notes also need to be obtained.

When a patient has a heart attack, usually the electrocardiogram is significantly abnormal, but was not in this case. This may not be abnormal in the first few hours but will often change. It did not change.

When the patient has a heart attack, with death of heart muscle, the proteins within these cells are leached into the blood stream and are measured by laboratory testing. This is the CK enzyme blood test. At 7:15 on April 10th, it was elevated to 263 with the normal range of 35-232. This can be from any muscle, but the specific fraction for heart muscle, called the CKMB, was significantly elevated to 9.6 vs. a normal range of 0-5.0. Thus, by 1715, it would appear, based on the blood testing, that the patient had sustained a heart attack.

The Emergency Room Department dictated report by Dr. #1 states that the total CK was normal, and I noted, it was not. He also states that the CKMB was normal, and again, it was not.

There is no mention that the patient had any complaints of chest pain in this portion of the emergency room record, nor in the admitting record. The patient had complained of dizziness, and apparently on that basis, a CAT scan of the head was obtained and showed a basal ganglia lacunar infarct. This was unchanged when the CAT scan was repeated the next day, on April 11th. Significantly elevated blood pressure can cause this type of a stroke in the deeper portion of the brain.

The patient's initial blood sugar was grossly elevated to 600, and during his hospitalization, he did receive treatment. He is a known insulin-dependent diabetic.

He had a number of studies of his heart. On April 11th, he had an echocardiogram which uses sound waves instead of x-rays. This showed that there was good contractility of the left ventricle (the main pumping chamber of the heart), and the ejection fraction, which is the pumping efficiency, was normal at 63%. On April 14th, he underwent a stress test that showed reversible ischemia (impairment of blood flow) to the anterolateral and inferolateral wall of the left ventricle. On this study, the ejection fraction was depressed to 42% (normal is 55% or more).

On April 17th, he underwent a cardiac catheterization procedure. This showed that the ejection fraction was above normal at 74%. There was only minimal atherosclerosis of the coronary arteries.

The patient did sustain a stroke that caused some difficulty with his speech and difficulty with his balance and ability to walk.

There are a number of complexities in this case, and let me give you the benefit of my analysis.

If he arrived at 10 o'clock in the morning and was simply allowed to sit in a waiting room with substantially elevated blood pressure (which they could not know what it was unless they took it), then the sustained high blood pressure, untreated, can increase the risk of a stroke developing. And by that evening, when the CAT scan was obtained, it showed evidence of an existing stroke that did not change by the next day. Since he had the neurologic deficit which was not of any long-standing nature, something happened either on the way to the hospital, or while waiting in the emergency room for medical care. But if he arrived at about five o'clock and was seen pretty quickly, then his blood pressure was treated rather rapidly with correct blood pressure lowering medication with a good effect. That will not reverse an existing stroke, but will contain one that may become hemorrhagic or extend.

Assuming they actually looked at the blood test at 1715, they could have treated the patient with TPA if, in fact, he had arrived and began treatment within four hours of the onset of his symptoms that, based on blood testing, are those of a heart attack. But if he had no chest pain, and simply elevated blood sugar, there is less of a rush to treat such a patient. Of course, they should have taken his blood pressure when he arrived in the emergency room since he was sick, but that outcome depends upon what time he actually arrived.

Assuming they would have begun therapy with TPA for his heart attack, it could also have had some effect on the thrombotic (blood clot) stroke. But when they had the results of the CAT scan of the brain that showed the lacunar infarct, there is some risk of treating such a patient TPA for the fear that it might convert it to a hemorrhagic stroke. There are some centers in this country at this time that are using TPA to treat acute strokes, but this is not a protocol available throughout the United States and is very controversial. It would have been even more controversial in April of 1998.

It appears that any damage with regard to his heart is minimal since, as the angiogram studies showed, his coronary arteries are fairly open, and that the heart muscle is contracting normally, and the ejection fraction is quite good on the best study that was obtained.

The best approach would be that if they did keep him in the emergency room without any blood pressure testing or treatment, and assuming the original blood pressure when he arrived was very high, then that would increase the risk of a stroke, which appears to be the major cause of his disability.

The defense would contend that since the CAT scan of the brain showed no change in the size of the lacunar infarct from April 10th until April 11th, it did not extend, nor did the patient's condition worsen neurologically, and therefore whether or not he would be treated with the controversial drug, TPA, really made no difference. And since the most definitive study on the heart (the cardiac catheterization) shows that the coronary arteries are fairly clear and there is no impairment of the pumping efficiency of the heart, the failure to treat him with TPA made no difference either.

So, in my opinion, it comes down to whether or not he had any neurologic symptoms before he arrived in the hospital, and how long he was maintained without any definitive treatment until after five o'clock. Therefore, it is essential to obtain the complete emergency room records with their nurse's notes intact and any blood tests and any other documentation from the emergency room, as well as the first two days of the nurse's notes in the hospital itself. We need to know what happened from 10 o'clock in the morning until 5 o'clock at night. Also, we need to know when his speech became abnormal, based on the patient's recollection and those of any witnesses, including his wife. According to the neurologist consulting with the patient, Dr. #2, he said, "No weakness except last night in the hospital he said his right hand was slightly tingly." And, "Today, April 11th, he noted that his right arm and leg were numb and weak 'as if he slept on it.'" Thus, it appears that there was a change that occurred on April 11th, and although the CAT scan was abnormal on April 10th, the progression of the stroke that caused symptoms was not apparent until the next day. Therefore, if his blood pressure was not treated and was markedly elevated during those seven hours of time, it may have increased the risk of the patient having irreversible changes associated with the stroke, as well as causing the stroke.

After you obtain those additional records, I will be pleased to review them, and then I would suggest that we have all the records reviewed by one of our experts in neurology to discuss negligence and causation, and then one of our experts in emergency room medicine with regard to the issue of negligence. Please advise us how you intend to proceed.

Addendum Report

The patient was 50 years old at the time he was admitted to the Hospital on April 10, 1998, for nausea and dizziness. The details of this hospitalization have been previously reviewed in the initial Case Evaluation Report.

Areas that have already been alluded to in the previous Case Evaluation Report that are still relevant include the fact that this patient was admitted from the emergency room at approximately 11 p.m. to the Surgical Intensive Care Unit. However, none of these records regarding nurse's notes are available from that hospitalization and Intensive Care Unit stay. The patient was hospitalized for a total of eight days, and therefore these records are indeed very relevant and the nurse's notes absolutely must be obtained to delineate the possibility of any medical negligence.

As indicated in the records, the patient had a history of poorly controlled hypertension as well as poorly controlled diabetes at the time of his emergency room presentation for weakness and dizziness. He was subsequently found to have a nontransmural, that is to say a subendocardial, myocardial infarction. This type of heart attack is one in which the EKG may in fact be misleadingly nonspecific, and yet actual cardiac damage did indeed occur as evidenced by an elevated myocardial enzyme known as the CPK-MB fraction. The emergency room doctor, Dr. #1, indeed had noted that the patient's CPK-MB fraction had been normal, and this is, in fact, a blatant misstatement of the facts. However, in view of the fact that this myocardial infarction was at the subendocardial level with EKGs before and afterwards remaining little changed, and a subsequent cardiac catheterization revealed minimal coronary artery disease, it is unclear to what extent this medical negligence resulted in any long-term sequelae.

Since the damages in relation to this misstatement with misdiagnosis are unclear, this act of negligence on the part of Dr. #1 would be very difficult to pursue, although it is clear that the standard of care for an emergency room physician seeing a diabetic patient with such symptoms was markedly substandard.

The patient was transferred to the Intensive Care Unit by Dr. #1 with a diagnosis of uncontrolled ketoacidosis (diabetes out of control). In reviewing the medical records, it is unclear whether the patient was administered any nasal oxygen as had also been the standard of care in relation to a diabetic patient with an abnormal CPK. In view of the patient's eventual demonstration that he developed or had evidence of a stroke, the lack of oxygen, if it can be documented due to negligence on the part of the emergency room personnel, would indeed have resulted in the possibility of further cerebral ischemic damage.

However, as mentioned, these emergency room records are somewhat vague and are scattered on numerous pages, and it is unclear to me if my initial impression is correct that the patient's emergency room visit, which lasted several hours, did not include the administration of oxygen. The emergency room care did, however, include prompt recognition of the patient's hypertensive emergency as well as the acute need to metabolically control this patient's hyperglycemic episode.

However, even though the patient's Emergency Room records do not seem to include the administration of oxygen, there is at least one entry which showed the patient had an oxygen saturation that is listed as 952, but this number is an obvious misprint, and the actual number will need to be more readily obtained.

As indicated in the prior Case Evaluation Report, the patient's ultimate degree of neurologic damage from his stroke may have much to do with his care during his first hours in the Intensive Care Unit. These details, such as the nurse's notes, are conspicuously absent in the reports received and will need to be obtained.

As mentioned, the patient underwent a cardiac catheterization procedure which showed an ejection fraction that was actually above normal at 74% with minimal atherosclerotic coronary disease. Therefore, it would appear that the effects that the heart attack had on the patient's actual cardiac contractility based on his catheterization report was indeed minimal. Nonetheless, additional details related to this patient's heart attack, as well as his possible role in the etiology of the patient's stroke, will also need to be obtained. However, since this heart attack was of a type known as a subendocardial infarction, there would have been no indication to the emergency room physician to have administered "clot busting" medications such as TPA or streptokinase.

The patient's development of renal failure appeared to occur prior to this April 1998 hospitalization at Hospital #1, but it was a marked worsening from his February 1994 Hospital #1 hospitalization. It is also unclear from the available records as to why the patient's renal functions had so precipitously declined in the interim and if any concerted effort on the part of his caretakers had taken place in the interim to closely monitor this patient's diabetes and hypertension control. Indeed, these additional outpatients as well as the already mentioned inpatient records are quite important to generate definite statements regarding causation in this case.

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