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Infectious Disease

• A Patient with Aplastic Anemia Develops Hepatitis C and Receives Unjustified Therapy for his Hepatitis Which Seriously Worsens His Anemia.
  
  
• Finger Injection Causes Infection; Delayed Drainage of Pus Destroys Tendon
  
  
• AIDS Patient with Pneumonia Receives Steroids and No Ventilator Which Causes Premature Death.
  
  
• Baby with Meningitis Misdiagnosed as Bladder Infection, Inadequately Treated, becomes Deaf.
  
  
• Diabetic patient develops an infection from a tetanus injection.
  
  
• Steroid injection given to sick patient based on misdiagnosis of allergies; develops severe pneumonia and dies.
  
  
• Abdominal (colon) surgery with failure to properly treat post-operative pneumonia and abdominal infection, causing death.
  
  
• HIV in a child treated with immune globulin and antibiotics, interrupted, and death from infection.

A Patient with Aplastic Anemia Develops Hepatitis C and Receives Unjustified Therapy for his Hepatitis Which Seriously Worsens His Anemia.

Aplastic anemia is an inability of the bone marrow to produce enough red blood cells, white blood cells, and platelets (clotting particles), and can be total or of varying degrees of severity. His was moderately severe and was controlled with GM-CSF (granulocyte monocyte colony stimulating factor) since 1991.

I have no records from his evaluation when he first was diagnosed with aplastic anemia at age 8. Sometimes it is caused by a side effect reaction to medications, and if they were not needed or not monitored properly, there may be another source of liability. Sometimes it is by a reaction to chemicals. Since he is not yet 21, you may also want to investigate this potential cause of action.

After he began his GM-CSF therapy, his aplastic anemia was under control where he no longer needed blood or blood component (platelet) transfusions.

Unfortunately he contracted Hepatitis C, which is a viral liver infection which becomes chronic. Depending on its activity, it can kill more liver cells than regenerate, resulting in scar tissue (cirrhosis), and liver failure. It can also cause liver cancer (hepatocellular carcinoma). The cause of hepatitis C infection is usually from an infected blood transfusion, or contaminated needle. 

I have no information as to how and when it was first diagnosed. The blood test for hepatitis C (non-A, non-B) is a few years old. But blood from paid sources, as opposed to volunteers, had a much higher risk for hepatitis C. 

Which source were his transfusions from, and how well were those donors screened? That is another potential source of liability.

The current drug therapy of choice for treating hepatitis C is Rebetron which consists of injections of interferon (Intron A) (an immune protein) and Rebetrol (ribavirin) (a drug that helps kill the virus). This combination of therapy has an approximate 40% positive response rate (significant reduction of the virus amount in the blood/liver), and decrease in liver cell destruction seen on a liver biopsy, twice as effective as interferon given alone. 

However, the FDA and the drug manufacturer warn in bold print: "The primary toxicity of ribavirin is hemolytic anemia (destruction of red blood cells)." They also state: " It is recommended that a patient whose hemoglobin level falls below 10 g/ (gram per decaliter) have his/her rebetol (ribavarin) dose reduced to 600 mg (milligrams) daily…. A patient whose hemoglobin level falls below 8.5 g/dl should be permanently discontinued from Rebetol/ Itron A therapy (see WARNINGS)."

When there is active hepatitis C the "viral load" (the number of viral particles per milliliter: ml of blood) is often one million or more. And as liver cells die from viral infestation they burst and their protein enzyme contents enter the blood, and are easily measured on standard laboratory tests. These are LDH, SGPT, and SGOT.

Before a patient is started on Rebetron therapy you need a reason, and often a liver biopsy is performed to actually determine microscopically what actually has occurred (scarring: fibrosis) and is (occurring active liver disease). With the standard needle biopsy through the abdomen into the liver, the major risk is bleeding, and if a patient has a very low platelet count (under 50,000, and especially under 25,000) it is contraindicated. 

A liver biopsy can be performed by threading the biopsy needle via a neck (jugular) vein, past the heart and via the inferior vena cava into a hepatic (liver) vein, which eliminates bleeding into the abdomen. That was done on 3/16/2001, 15 months after the Rebetron therapy was terminated (after two weeks of therapy), and revealed "mild to moderate chronic periportal inflammation," and "mild porotal (the vein that brings blood into the liver from the intestines) fibrosis (scarring)." "The hepatic lobules (liver cells) are otherwise unremarkable)." This is not significantly active disease.

In his case, all the liver enzyme blood test were all normal on six studies form 7/98 through 1/3/00 and also on the eight studies after his Rebetron therapy through 10/2000 (and some were even below normal). All evidence against significantly active liver disease.

The Hepatitis C viral blood levels were 564,000 on 4/97, 700,000 on 7/13/99 and 330,000 on 11/18/99.

His hemoglobin blood levels (the oxygen carrying red blood cell pigment) showed significant anemia for years, as well as on 1/3/00 at 8.1. This is obviously below the 8.5 warning threshold level to terminate the use of this drug (ribavirin).

I know of no studies that evaluate the risks and benefits of Rebetrol in patients who have hepatitis C and aplastic anemia. Therefore, this is experimental and requires a very stringent level of informed consent.

Based on the normal liver enzymes and moderate level of hepatitis C viral particles there would be a question of therapy without a liver biopsy. But in a patient also with severe anemia, I believe that it was a departure from the standards of care to begin Rebetron therapy on 1/3/00.

On 11/18/99 they noted that the HCV (hepatitis C) PCR (viral blood level) was "700,000 copies" on 7/99. But they (Dr. #1, Dr. #2 and FNP Family Nurse Practitioner #1) never noted the 330,000 HCV PCR level that was done on 11/18 until 1/3/00, and did not stop initiating the "therapy."

On 11/22 FNP #1 noted that both Drs. #1 and #2 recommended a platelet transfusion and percutaneous liver needle biopsy (into the abdomen) "before interferon therapy versus Interferon / Ribavirin therapy." They were also going to do a bone marrow aspirate biopsy. "he should also be followed by Hepatologist (Liver Specialist) for Hep C therapy." I found no such consultation. Also it was not the interferon that caused the worsening of his anemia. It was the ribavirin. Although interferon has one-half the response rate, it could be given alone. In addition, a better form of interferon, Pegasys was under development, and there was no rush in his case to begin any risky therapy.

He returned on 1/10/00 FNP #1 noted "His CBC (complete blood count) has fallen a lot since last week, but he says he forgot to take his GM-CSF last night. I emphasized to him that the Rebetron has cause some decrease in CBC and he needs to take GM-CSF every night. We will probably go up on dose next week if CBC is still decreased." There is no evidence that this negligent FNP ever brought any of this to the attention of her supervising doctors that day, or ever. His Hgb (hemoglobin) level was down to 7.7 and his white blood count was dangerously low at 1.8 (1,800) versus 2.7 the week before. He was at a serious risk for infection.

On 1/17 his Hgb was 6.0 his platelet count dropped from 16 (16,000) to 9,000 in one week. This FNP and Dr. #2 still did not stop the Rebetron therapy.
On 1/19 the Hgb was 5.6 and the platelets only 10,000. Finally the Rebetron therapy was stopped by FNP #1 and apparently some doctor (whose signature I cannot read). On 1/19 transfusions were ordered to begin with two units of RBC (red blood cells). He also was transfused two units of RBC on 2/7, 2/21, 3/14, and 4/4.

The bone marrow makes all these blood elements and some of the immature red blood cells, called reticulocytes, enter the bloodstream. His reticulocytes count pre-Rebetron on 7/12/99 was 3.0, 11/18/99 1.4 and on 1/3/00, the day of initiation of Rebetron, it was 2.6 Then it dropped to 0.6 on 1/10/00 and further decreased to 0.2 pm 1/19. On 1/31 it was 0.9. This is the opposite response of the body to hemolytic anemia where red blood cells are destroyed, and a healthy (functional) bone marrow makes more cells. This is evidence of a direct toxic effect of ribavirin on his bone marrow. Did his doctors report this to the FDA as they should have done, and did they publish their finding in any medical journals to warn other doctors of this danger?

Apparently, he will undergo a bone marrow transplant. That will complicate his hepatitis C depending on which additional drugs he will receive. Immuno-suppressive drugs do interfere with the body's ability to fight infection, including viruses. And with a damaged liver, many drugs are more toxic to his liver.

He is at risk from bleeding internally and externally from a very low platelet count. He is also at risk from complications from blood transfusions including infections and transfusion reactions. 

The Defense will content that he was fully informed of all the risks, but what known risks are there with aplastic anemia, to fully inform a patient about? I now of no information on that subject. You may want to conduct a Medline search (with the National Library of Medicine)
Using the key words ribavirin and aplastic anemia. 

The Defense will try to claim "contributory negligence for him missing one dose of GM-CSF on 1/9/00. I doubt it made the difference to his persistent bone marrow suppression.

Since 3/4/96 has he ever missed taking any of his daily 250 mcg (microgram) injections? If so, there did not appear to be any profound effect on his bone marrow and anemia.

In my opinion Dr. #1, Dr. #2, FNP #1, their hematology clinic, and Hospital #1 (which appears to be their employer or created agents of them) are all negligent for all the reasons stated above.

You need to know that there are nutritional (herbal) alternatives to aid the liver including milk thistle (containing silymarin), and combinations of Chinese herbs. Was this option with no side effects ever discussed with him?

I would suggest that you authorize our office to obtain Board Certified Experts in Hematology, Infectious Disease and Gastroenterology to give you their opinion on negligence, causation, and damages.

He also was noted to have a probable panic attack" on in 3/00. Has he been under a Psychologist or Psychiatrist's care?

Thank you for allowing our organization to assist you with this interesting case. We continue to remain available on this case to obtain Expert Witness opinions.

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Finger Injection Causes Infection; Delayed Drainage of Pus Destroys Tendon

This 43-year-old working man developed some "triggering" of the fourth finger on his right hand. This occurs when there is swelling involving the tendon and the sheath (like a pulley) through which it passes. The initial treatment is rest, elevation and some anti-inflammatory medications. 

If the problem persists, then a steroid injection of sterile medication under the most sterile conditions is acceptable. As you noted all those records are not available.

His finger began to swell, was painful, and inflamed after three days. One week after the injection he saw Dr. John on 6/1 where this problem was noted and he apparently had been taking the antibiotic erythromycin and the pain mediation percocet, without relief.

An infection from a finger injection is potentially very serious because it can destroy the tendons and their pulley sheaths as occurred here, and can also spread into the hand and via the tendon sheath, into the other fingers and wrist, which did not occur. Also, the joint can become infected, which also did not occur.

You noted that Dr. #1 sent the patient to the E.R. for an antibiotic injection (Rocephin), and placed him on a more potent oral antibiotic (Cipro) for two weeks and a narcotic (Percodan) for pain. He did not aspirate the infected area (using a needle and syringe) to look for pus and culture it to find the nature of the germ and the best antibiotics to kill it, nor did he open up the would to drain this obvious infection which was caused by the injection the previous week, nor did he obtain a consultation, or an MRI of his hand. The failure to intercede in my opinion is a departure from the standards of care.

The best opportunity for minimizing the devastating effects of the infection was lost. I am missing that E.R. record. Was he seen by the E.R. doctor? If so, that Physician, E.R. Corporation and hospital also would be negligent.

On 6/21 his fourth finger was "hot to touch, swollen and inflamed" and the next day he was seen by an Orthopedic Surgeon, Dr. #2, who felt that: "It appears that the infection is under control." Obviously it was not, and nothing would make such a major difference in this severe infection in one day. In my opinion, based on the history and previous day's findings, all of the previously mentioned care should have been undertaken.

She noted in her 6/29 office record that he had increasing symptoms that required I & D (incision and drainage).

Finally he was hospitalized for surgery on 6/29 by Dr. #2, and on 6/30 he had the superficial (sublimis) flexor tendon excised because it had become gangrenous (necrotic) from the infection. Also "the flexor profundus (deep tendon to the end of the finger, and the more important one for full flexion) was intact but without blood supply presumably across the area of the necrotic sublimis" which predicted that it too would die (gangrene). She excised the necrotic sublimis tendon and sutured the wound closed loosely over a drain. The surgery was acceptable, but weeks too late!


Although no germs grew out by laboratory analysis, they were seen under the microscope (gram stain). The antibiotics helped to kill most of them, but not before all the damage was done. Tendon has a poor blood supply, and infection will clot off (thrombose) its fine blood vessel supply, resulting in the necrosis that occurred, and the dying and dead flesh will promote infection. Also, the initial steroid injection will depress the local area of the body’s ability to fight infection. That is also why earlier diagnosis and intervention is needed.

In my opinion there was the potential for an unsterile injection by Dr. #3 depending upon how thoroughly the finger cleansed and with what antiseptic prior to the injection, the sterile maintenance of the steroid if it was a multi-dose vial, its manufacture, and the technique used. Skin and its sweat glands do contain germs and they are not always eliminated by antiseptics, allowing the needle to drag them deeper.

When he presented to Dr. #1 one week later, that care was negligent in my opinion for all the reasons stated. The delay of one additional week by Dr. #2 may have made the difference in saving the profundus tendon.

It looked as if the infection was going to resolve but required further drainage and excision of dead tissue (debridement) on 7/13. An attempt to reconstruct the tendon pulley was performed, but would have minimal success in the midst of that infected and inflamed flesh (tissue), and placing sutures (foreign bodies) under those circumstances is highly questionable, and can worsen the infection and its consequences. It failed.

On 7/21 Dr. #4 was consulted and created a splint.

On 9/13 Dr. #2 removed 3 cc (1/30 of an ounce: 3/5 of tsp.) of pus by needle aspiration.

On 9/15 Dr. #4 noted that his flexor digitorum profundus (FDP) tendon function was intact at that time.

But on 10/22 he operated and excised a necrotic deep profundus tendon confirmed by the pathology report. Germs (coagulase negative staphylococcus) were present in this chronically inflamed wound that had never fully healed.

After adequate time for the infection to resolve, Dr. #4 operated on 4/4 to insert a silicone rod from the wrist area into the finger to help create a tunnel through which a tendon graft could be placed, months later. He also used a piece of wrist tendon (palmaris longus) to reconstruct the pulley sheaths in the finger that were destroyed by the infection.

The on 11/10 he used a piece of foot tendon to serve as the new profundus tendon and placed it in the sheath by attaching it to one end of the silicone (Hunter) rod as he removed it, and sutured each end to recreate a functioning flexor muscle / tendon/ finger unit.

In my opinion, all the care by Dr. #4 was quite good.

The main negligence as the cause of the devastation was caused by Dr. #1 with one questionable week by Dr. #2. I raised concerns re: Dr. #3.

What is his present hand function? Obtain photographs with his hand opened and closed.

I would suggest that you authorize us to obtained Expert Reports by Physicians specializing in Hand Surgery, Infectious Disease, and the same specialty of Dr. #1 (whatever that may be).

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AIDS Patient with Pneumonia Receives Steroids and No Ventilator Which Causes Premature Death.

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 Hospital 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 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 aterial 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 oxygen 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 Board Certified Experts in Pulmonary Medicine, Emergency Medicine and Infectious Disease for their opinions as to the care at this Hospital and those Physicians, as well as try to determine his AIDS status and potential longevity. 

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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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Diabetic patient develops an infection from a tetanus injection.

The patient was a 57-year-old, obese, noninsulin dependent diabetic, who sustained a second-degree burn (blister) on her left wrist. Her last tetanus immunization was six years before, and therefore it was reasonable for her to receive a tetanus injection.

What did the Nurse use to sterilize her skin? Was the tetanus toxoid from a one-shot/prefilled syringe? Was it drawn up, via a needle, into a syringe by the nurse from a one-dose vial, or from a multi-dose vial? And, if so, was this the first dose withdrawn? How was the rubber stopper sterilized before the needle punctured it, and how was it refrigerated between uses? Was it used on other patients, and did it cause any infections in other patients?

If there were failure in any of these sterile techniques, then that would be negligence and markedly increase the risk of this patient developing her infection. Did the Board of Health conduct an investigation? If so, obtain their investigation report.

However, if all of the above was done properly, an infection developing at an injection site is not necessarily from negligence. There are germs in the skin sweat glands that are not always sterilized.

Her fever to 103 degrees and chills, plus blister formation at the site of the injection is consistent with an infection. However, the normal white blood count and differential smear (the type of white blood cells) are evidence against any severe infection, although diabetics do have a subnormal immune system and may not react with a significant rise in their white blood cells to a localized infection. Also, the two samples of her blood were evidence against a serious blood-borne bacterial infection (sepsis).

She was hospitalized for four days and received intravenous antibiotics (vancomycin). That hospital care was good.

She had a history of congestive heart failure and was seen in the emergency room two years earlier complaining of shortness of breath (S.O.B.), consistent with congestive heart failure. She was receiving a potent diuretic medication (Lasix) at the time in question.

In her statement of facts, she notes that she had disabling persistent pain for at least six months (to the present time). I have not seen the subsequent hospital records from Hospital #1 of 10/27 and 11/12, or the office records of Dr. #1 from 10/29 and 11/15. I have not seen the specialist's records from the Hospital #2 of 12/16 and 1/3 of this year.

Also, is anything visible now on her arm? If so, obtain close-up photographs from different views. Were any photographs obtained earlier? Send copies.

She complains of pain in the entire side of her body in which she received that tetanus toxoid injection. That does not make medical sense, in my opinion. She complains of pain in her ankle, leg, and hip; that also does not make medical sense with regard to an infection in her arm, in my opinion. Nor do the migraine headaches or inability to shop or pay her bills.

If she had developed an infection, and if she developed chronic pain at that site which was supported by subsequent evaluations (which I have not yet seen), then there would be "causation for that problem." If the Nurse failed to follow the sterile procedures I noted above, then there would be negligent care.

Please supply answers to all the questions I have raised, and all the missing records in order for me to finalize my opinions. Then I would probably recommend Experts in Nursing, Emergency Room Medicine, and possibly, Infectious Disease.

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Steroid injection given to sick patient based on misdiagnosis of allergies; develops severe pneumonia and dies.

This 45-year-old man had the "flu" for three days, with a sore throat, chills, a productive cough (color of sputum unknown) and 103-degree fever. His lungs were "clear" at that time. He was evaluated by a physician (whose signature and second person's signature is not legible) from the Clinic, on 12/29. At that time they noted his respiratory rate was 16 (normal) and his temperature was 101.

He was given an injection of Celestone (betamethasone) (1.5 cc = 9 milligrams) intramuscularly. This is a very potent steroid drug. He also received a prescription for Allegra (for allergies) and an illegible medication. The "assessment" was "flu." I agree.

Steroids depress the immune system thereby making it more difficult for a patient to fight infection. He had "sinus" under the "review of systems" but no notation of pain in the sinuses. There was no evidence of allergy. He did not have asthma. The lungs were "clear," not full of wheezing breath sounds.

The F.D.A. and drug manufacturer of Celestone note that for "Allergic states: Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment…." He had no other therapy that failed. In my opinion injecting a potent steroid into this patient was a departure from the accepted standards of care and denied him a better chance of fighting his infection (flu that they diagnosed), which in combination with the steroids, weakened his lungs and allowed a severe streptococcal bacterial infection to cause pneumonia.

If steroids were needed, then the standard of care is to give it every 12 hours. He had a one dose "shot." Doctors earn income from injections and office visits, not prescriptions.

Determine what that illegible medication he was prescribed or given on 12/29.

The next day, 12/30, at 7 a.m. he came to the Emergency Room with a temperature of 104.2, blood pressure of 102/70 (low), pulse of 136 (fast) and respiratory rate of 38 (three times normal). He had gotten worse at 3 a.m. and had increased shortness of breath (SOB) at 6 a.m. The chest x-ray at 2:30 p.m. showed: "Extensive right upper lobe pneumonia persists." It worsened to involve both lungs.

Because of severe respiratory failure, shortly after admission to the hospital, while already receiving intensive intravenous antibiotics, he was transferred to the Intensive Care Unit (I.C.U.) for the insertion of an endotracheal tube: intubation (a breathing tube inserted into his windpipe) and he was put on a ventilator.

The tube was needed and did not cause his pneumonia. However, the patient had to be sedated and paralyzed with drugs in order to effectively ventilate him. He could not cough and that does increase the risk of pneumonia, even though the nurses were suctioning out the mucus from his lungs via that tube.

He went into septic shock (the streptococcal bacterial germs, and its poisonous by products overwhelmed his body's defenses) within one day, and he developed kidney failure and had a dialysis treatment. He was alert initially, but developed progressive coma. His skin began to peel off his body.

Even with very high-pressure settings on the ventilator to prevent his lung air sacs (alveoli) from collapsing with the P.E.E.P. (Positive End Expiratory Pressure), his lungs were losing their ability to transport oxygen. With family consent the endotracheal tube was removed and his blood pressure raising medication stopped. He died on January 4th from his overwhelming pneumonia, despite proper in-hospital care and many consultations.

The admitting physician was Dr. #1. He noted, "he was seen in the office." Was he the doctor who prescribed the steroid injection? That doctor and the clinic should be defendants.

The defense will contend that he had only one injection of the steroids for sinus problems. But he had 103 degree fever, and if he had a sinus problem, it was a severe infection. Those germs would enter his lungs via his breathing and his lungs' ability to fight that germ infection would be impaired from this very potent steroid which should not have been given.

What is the background and training of that doctor in the clinic? It he Board Certified in Family Practice? Did he ever fail his board examination?

I would suggest that you authorize us to obtain an Expert Opinion from an Infectious Diseases Specialist and then a Family Practice Expert.

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Abdominal (colon) surgery with failure to properly treat post-operative pneumonia and abdominal infection, causing death.

This patient was 79 years old at the time he was admitted to Hospital #1 on January 6, for evaluation of dizziness and anemia. A CAT scan of the abdomen obtained at that time indicated a colon lesion which was subsequently evaluated by colonoscopy on January 7. The colonscopic biopsy revealed adenocarcinoma as well as a polyp. The procedural issues regarding the colonoscopy appear to be within the appropriate standard of care although I am unable to find documentation that pre-biopsy antibiotic prophylaxis was administered. The reason that antibiotic prophylaxis is generally recommended prior to colonic biopsy stems from the observation that a subset of patients who undergo this procedure will sustain bloodstream infections in the aftermath of this procedure or may suffer other infection complications for which antibiotic prophylactic therapy is beneficial. However, as mentioned, it is unclear from the available records whether this antibiotic prophylaxis was given, but there did not appear to be any direct consequences, even had this prophylaxis been omitted.

Following the January 7, finding of adenocarcinoma of the colon on colonoscopy, the patient was scheduled for a surgical right colon resection, which he underwent on January 8. The surgical procedure note performed on that date by Dr. #1 revealed that both a hemicolectomy and cholecystectomy were performed, the latter for diagnosis of a chronic cholecystitis, and antibiotic prophylaxis was ordered, although it is unclear whether the antibiotic (cefazolin) was ever administered within the recommended one hour preoperative timeframe.

Procedural details are somewhat scant, but it appears that the patient tolerated the hemicolectomy procedure without untoward complications until the following day on January 10 when a fever was noted, in the range of 102 degrees (39.0 degrees centigrade). The workup for this temperature elevation was substandard with a lack of blood cultures, chest x-ray, urinalysis, urine culture or an attempt to obtain sputum culture or abdominal follow-up CAT scan.

It can be stated within a reasonable degree of medical certainty that in a 79-year-old patient who had undergone a colon resection procedure that a high index of suspicion for postoperative complications, such as infection, should have been maintained. Indeed, as stated in numerous studies on postoperative infectious complications from intra-abdominal surgery, an aggressive workup with expeditious use of empiric antibiotic therapy directed against the most likely causes of such fevers is essential to avoid catastrophic complications, such as those that were observed here.

It can also be stated, within a reasonable degree of medical certainty, that the lack of aggressive workup and early use of empiric antibiotics contributed significantly to this patient's adverse outcome. Indeed, on January 11, his temperature rose further in the range of 40-plus degrees centigrade. The temperature elevation on January 11 was also accompanied by a markedly substandard workup of this fever and no antibiotics were prescribed for multiple days beyond the occurrence of this temperature elevation. In fact, the prescription of acetaminophen, or Tylenol, although not a deviation from the standard of care in its own right, masks the temperature parameter that is so essential to follow in these cases. In addition, the follow-up by Drs. #1 and #2 in the setting of this fever was markedly substandard with no Internal Medicine or Surgical follow-up on many of these days.

If it is indeed documented to be that no follow-up examination or history was afforded the patient by Drs. #1 and #2 on these dates, then additional serious deviations from existing surgical and medical care occurred, which, more likely than not, also contributed significantly to the patient's eventual adverse outcome. Indeed, the patient's temperature elevation became more difficult to assess while on the acetaminophen but never fully normalized throughout the remainder of his hospital stay. Also, there was no blood gas determination for him until the day of his demise, and oxygen therapy was also delayed and inadequately administered. In addition, there is an order to obtain a chest x-ray that was dated January 13 for that day, but the chest x-ray obtained did not occur until the following day on January 14.

On January 14, at 11 a.m., the patient was noted to be disoriented, and by the time antibiotics were administered, an additional period of over an hour had elapsed. The antibiotic Timentin was ordered, but it is unclear at what time this was actually administered. What is clear is that the patient, who had had postoperative fever for over 72 hours, only received the benefit of a single dose of this antibiotic prior to his death on the afternoon of January 14.

Although it is not fully clear whether the patient's death was due to a hospital-acquired pneumonia alone or in conjunction with an intra-abdominal infection, it is clear that the patient's medical and surgical evaluations and the use of empiric antibiotic therapy were delayed and inadequate. In fact, a delay of over 72 hours without an adequate workup to delineate the cause of this patient's fever evidences markedly substandard care which had a major impact on the prognosis of this 79-year-old patient. Both hospital-acquired pneumonia and postoperative intra-abdominal infections are treatable and curable conditions when recognized and diagnosed at an early stage.

It can be stated, within a reasonable degree of medical certainty, that any fever in the setting of recent intra-abdominal surgery with an abnormal white blood cell count and differential count, should have been considered to be due to infection until proven otherwise. Such a management strategy would have resulted in early diagnosis of a lung infection with or without intra-abdominal sepsis and empiric early use of antibiotics, which should have prevented this patient's multisystem dysfunction and eventual death.

The condition known as hospital-acquired pneumonia carries a mortality that approaches 100% when undertreated or underappreciated, as was the case here. Since the majority of cases of hospital-acquired pneumonia are due to an aggressive type of bacteria referred to as gram negative rods, the standard of care for such a condition generally calls for two antibiotics directed against that bacteria. The use of a single antibiotic in the form of Timentin, which is ticarcillin with clavulanic acid, constituted essentially a single drug which also represents a deviation from existing standards of care.

In summary, although the colonoscopy and the colectomy as performed on the patient appeared to be medically indicated, the postoperative fever that he developed was inadequately managed, both diagnostically and therapeutically. This not only constituted a marked deviation from the existing standards of care, but contributed significantly to his adverse outcome and death.

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HIV in a child treated with immune globulin and antibiotics, interrupted, and death from infection.

This is a complex case from many facets, as I shall describe in detail below.

At age 3 1/2 years old this HIV infected child since birth died from sepsis (spreading infection throughout the blood and body) from the germ Streptococcus pnemoniae that was documented to be in the lung and spinal fluid at his autopsy and in his blood in the Emergency Room.

All the Emergency Room care was excellent, but he was really dead on arrival with his arrest occurring earlier in his mother's car. Despite all the proper resuscitation efforts he was beyond help. The venous and then the arterial blood test revealed that the blood acid level was 6.5 which means that a prolonged time without adequate ventilation and cardiac massage had occurred.

The autopsy also revealed abscesses in his lungs and liver consistent with the diagnosis of sepsis. The autopsy did not evaluate the implanted intra-venous device (port-a-cath) which possibly may have been the site of infection, but previous examinations did not find it to be a problem.

His intellectual and physical developmental delays had substantially resolved.

On February 3, Dr. #1, an Infectious Disease Specialist treating him prepared a 4 page letter concerning his care and her recommendations, and gave this document to his mother. She noted that he had not received any anti-viral (HIV) therapy since for two years but "His absolute CD4 count has remained relatively stable within the moderately immunocompromised range...". The mother did not want to resume that therapy, and follow up testing would be done.

On 9/8 the previous year the antibiotic Bactrim (TMP-SMX) was discontinued but restarted on 2/3 as prophylactic treatment for PCP (Pneumocystitis carni) infection that is a danger to HIV positive patients.

Dr. #1 noted "Twice daily amoxicillin for prophylaxis following his splenectomy. Removal of the spleen was indicated for his low platelet (clotting particle) count but increases the risk of infection by bacteria and sepsis. He was also receiving IVIG (immune globulin injections) every 3 weeks via his port-a-cath. He was to get a dose on 2/4. She recommended that this IVIG be continued, and planned to give him a dose in April "right before they left the state". Did he get that dose? (see below re: 4/30).

Most importantly to this case, Dr. #1 recommended he resume "receiving amoxicillin bid (twice a day) as prophylaxis against overwhelming sepsis with encapsulated bacteria (which includes Streptococcus pneumoniae) following his splenectomy". Dr. #1 said his mother "prefers not to give amoxicillin".

In the second state he came under the care of Dr. #2 who saw him on 5/13 and 5/28. He noted on 5/13 that the last dose of IVIG was on 4/30. He was going to call to check on restarting the IVIG. He also spoke with Dr. #3 (apparently a Hematologist) and said the IVIG was not needed regarding the platelet count which was normal at 380,000 but to check with an Infectious Disease Specialist regarding prevention of infection. He spoke with Dr. #4's office to get his records on 5/14 and on 5/17 and consulted with Dr. #5 regarding the CD4 count of 19% (unchanged from February where it was 18%). The laboratory results were faxed to Dr. #5 on 5/17 and Dr. #2 was still waiting for the records. All this is good care.

During the office visit of 5/28 the patient was "happy playing", the ear drainage tubes were properly "in place". There was some nasal congestion but the chest was "clear". He had some insect bites and a localized allergic (urticarial) reaction. This was treated with a steroid cream and antihistamine; proper care. And he was "awaiting further recommendations from Dr #5". Again, proper care.

On 6/9 "Dr. #5 sent an e-mail recommending that patient re-start amoxicillin prophylaxis for post splenectomy patients...". He called the patient's mother and left 2 messages on her answering machine. Again, proper care. This was not an emergency since he had not received this antibiotic since the previous summer.

On 6/11 or 6/12 his mother spoke to Dr. #2 and agreed to re-start the Amoxicillin as well as the IVIG. This was planned to be discussed at the next office visit scheduled on 7/6. This was reasonable.

During the day on 6/25, about noon he was sleepy, vomited, began to run a fever or 103 or 104 and had an "unusual breathing pattern". She was unaware of ambulance services so she began to drive him the hospital and he arrested on the way.

Based on all the above, I believe that the patient received good medical care. He was not "sick" when he saw Dr. #2 on the two visits and had been off the Amoxicillin antibiotic for one year. His sepsis was very sudden and unfortunately he did not reach the Emergency Room in time for their good care to have an effect.

Possibly one of our Infectious Disease Experts may conclude that his treating (and consulting) physicians should have insisted that he continue to receive the IVIG and amoxicillin therapy without any interruption. And if that is his opinion, he would be able to try to tell you what difference it would have made to his immediate survival. Also, that Expert could try to advise you what his ultimate chance for survival with him being HIV positive at age 3 1/2, based on current drug therapy and what may be available in the future.

He was going to be referred to a Dentist. Did he have the dental work done? If that occurred without antibiotic protection, that would be negligent and increase the risk of sepsis.

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