LL Part 3: Death already lived in the NICU Environment
Is there any link between baby deaths and the plumber's evidence?
Following on from the previous post (here)
Revelations from the ongoing trial of British nurse Lucy Letby have created many more questions than they have answered regarding the cluster of neonate deaths that occurred at the Countess of Chester Hospital (CoCH). While we do not know the reason for his decision, Lucy Letby’s barrister Mr Ben Myers KC elected to only call one witness in Lucy’s defence - Mr Lorenzo Mansutti. The plumber.
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It has been widely reported that all Mr Mansutti gave was corroborating evidence about a single instance of hospital wastewater (HWW) flooding in the neonatal unit. Others point out that, as the prosecutor sought to paint, much of the remainder of his evidence was about the wards next to and above the neonatal unit which the prosecutor got him to say could not have affected the neonatal unit. But is this the case? And is there a more fundamental reason why the management at CoCH decided to repair and replace a whole heap of plumbing in 2016, ahead of spending £3mil to build a new and expanded neonatal unit?
Does building the new unit on the old NICU site mean this couldn’t happen at CoCH again?
Pathogens in Hospital Wastewater (HWW)
The evidence Mr Mansutti gave in court set this researcher on a particular path of investigation, because buried within it were several interesting clues. While Mr Mansutti corroborated Lucy’s statement that HWW had seriously flooded the neonatal unit on at least one occassion, his evidence also told us that there were issues with HWW in the building during the entire 2015-2016 period (and that being the case, likely for some time before), that plumbers were resolving blockages and leaks in the building during this period on a weekly basis, and that there had been more than one serious flood in the unit. It also told us that blockages, leaks and cracks in the 50+ year old cast iron pipes had occured in the wards around the neonatal unit - but especially the one above the neonatal unit - potentially allowing HWW to drip down into the neonatal unit or resulting in pathogens being aerosolised into the neonatal unit environment. And finally, that the computer system the hospital used to maintain record these incidents was incomplete, because incidents had occured that were not recorded in it and what information was in it did not adequately reflect the truth of the issues experienced on the ward.
Hospitals are singularly notorious for causing infection in patients while treating them for something else. We even have a term for this… nosocomial infection. The word nosocomial specifically refers to a disease the patient did not have when they came to the hospital. An infection that originated in or was acquired while they were in the hospital facility.
The most commonly discussed nosocomial infection is Methicillin-resistant Staphylococcus aureus (MRSA), an antibiotic-resistant form of what was sometimes referred to as golden staph. S.aureus is a normal part of the bacterial flora of many of our bodies (while most people carry the bacteria under their arm pits and in their groin and skin folds, around 20-30% of people’s noses are also colonised with S.aureus at any given time). A key difference between S.aureus and the other pathogens I am going to discuss here is that while golden staph. and MRSA became household names and received significant attention in the media, hospital internal training programs and medical and nursing courses… the ones I describe below get fleeting mentions here and there and very often are not even mentioned in hospital in-service training courses1.
There are many differences and similarities between the three primary HWW pathogens I will discussed in these articles. Children under the age of 3 months, and especially premature and low birth weight neonates, are already at significantly higher risk for serious bacterial infections. While some studies have found that there can be common presentations across two or more, such as infective endocarditis, others report very distinct clinical presentations for each that we will relate to the symptoms of several of the neonates later in this series.
In each case the neonate may appear to have no symptoms (known as a silent infection), one symptom, or a number of these symptoms identified on careful clinical examination. Each symptom can also be confused with being its own pathology, or as part of the presentation of several other diseases. And often, unless you have seen it before, as a nurse (or even a doctor) you might not realise that one (or more) of these pathogens are actually ‘in play’.
Enterococci are Gram-positive bacteria that inhabit the gastrointestinal tracts of humans and many animals. They are among the major causes of nosocomial infections and are found in the HWW of most hospitals. Enterococci are one of the most commonly identified causal microorganisms from hospital acquired bloodstream infections. They can persist in the hospital environment for extended periods, tolerate a wide range of temperatures, can be transferred unwittingly between surfaces such as incubators by healthcare worker’s (HCW’s) hands, and are often multi-antibiotic resistant. NICU rooms can be reservoirs for Enterococci, explaining how multiple neonates in the NICU can be colonised by the same strains either at the same time or across many weeks or months. Outbreaks can last across several months and persist even after several different mitigation measures are employed.
Vancomycin-sensitive Enterococcus faecalis (VSEfe) outbreaks are difficult to recognise and may only be identified when there is a clustering of cases. Procedures such as staff changing diapers inside the confined space of the cot and pushing the soiled diaper to the side or bottom of the cot before disposal can unwittingly contaminate the internal and external cot environment. Given that many neonates are catheterised, colonisation from cot to skin could then provide access for microbes to enter the blood stream. Cleaning procedures must be meticulous because Enterococci contaminate the hospital environment and equipment easily and persistently. When identified, infected neonates should be isolated from other infants and cared for under strict hygiene controls because in spite of treatment, aberrant colonisation of the GI by Enterococci can be persistent.
Enterococci such as E. faecalis are one of the first bacteria to colonise the newborn’s gut after birth, and are necessary for proper development of our gastrointestinal (GI) tract. Infections involving Enterococci include acute bacterial meningitis, neonatal sepsis and catheter-related bloodstream infections that can lead to intestinal failure, urinary tract infections (UTI), endocarditis, wound infections and central nervous system (CNS) infection. These bacteria are also frequent causes of late onset bacteraemia and sepsis in NICU patients, which is generally nosocomial (hospital acquired). Most neonates who succumb to Enterococci infection have had prior antibiotic therapy and multiple invasive procedures.
However, around 75% of cases of necrotising enterocolitis (NEC) seen in hospitalised neonates are caused by aberrant microbial colonisation with Enterococci - that is, the bacteria colonise places other than where we would expect them to be. NEC’s clinical presentation can be non-specific, and can include feeding intolerance, the absence of contractions in the intestines (ileus), the accumulation of air in the abdomen (abdominal distension), and even the observance of fresh blood in the neonate’s fecal matter (haematochezia). Where NEC progresses to multiorgan failure neonates can present with lethargy, reduced frequency and even the complete absence of breathing (apnoea), the buildup of acid in the body usually caused by kidney disease or failure (metabolic acidosis) and abnormal clotting throughout the neonate’s blood vessels (disseminated intravascular coagulopathy or DIC). The most common characteristic of NEC observed on x-ray are pockets of air in the abdominal space outside the intestine (pneumatosis intestinalis) and accumulations of air in the main blood vessels that drain blood away from the gastrointestinal tract and visceral organs known as the portal vein (portal venous gas). Low birth weight and prematurity are key risk factors for NEC.
Pseudomonas aeruginosa is a gram-negative bacteria commonly found in soil and water, and a common nosocomial acquired pathogen that infects respiratory and urinary tracts. P. aeruginosa is ubiquitous in hospital wet areas and on taps and sinks, and anywhere that is humid such as inside and around respirator equipment. It’s ability to build a biofilm on and inside surfaces has seen it become disinfectant resistant and found responsible for 15% or more of all nosocomial infections. Infection with Pseudomonas may not always be identified in the laboratory as it is not generally considered a pathologic finding.
Several outbreaks of Pseudomonas have occurred in intensive care and neonatal units in England and Ireland. Pseudomonas outbreaks have occurred in hospitals with longstanding slow drainage of HWW, frequent foul smells emanating from drains and basins, buildings and bedpan sluices with recurring problems with blocked sewage pipes leading to backflow of HWW. It is not uncommon for patients to be erroneously blamed for bringing Pseudomonas into hospital wards, even though outbreaks resulting in patient deaths have been traced to such unlikely and unwitting sources as: (i) pharmacy-supplied sealed bottled water brought into the intensive care unit to prepare medication administered via nasogastric tubes; (ii) neonatal nurse’s manicured fingernails; (iii) faulty hospital sink, shower and toilet design; (iv) clean items like bedlinen stored near sluices; (v) contaminated medications; (vi) respiratory equipment; (vii) laryngoscopes; (viii) inconsistent handwashing techniques; (ix) contaminated hospital water; and (x) frequent blockages and leaks from wastewater pipes. Biofilms of Pseudomonas have previously been identified in the pipes bringing fresh water to hospital hand basins however, even after mitigations had been performed and faucets had been replaced, a second cluster of cases occurred in the same NICU (Kinsey et al, 2017).
Neonates are particularly vulnerable to Pseudomonas infection because of their underdeveloped immune systems, limited skin barrier function, catheterisation, and exposure to invasive procedures and devices. As we saw in yesterday’s article, until nurses, doctors and hospital management recognise that a cluster of deaths might represent an outbreak, Pseudomonas can hide in the ward and unchecked will result in the deaths of many of our most vulnerable patients. As with the other HWW pathogens, neonates who succumb to Pseudomonas are more likely to be premature and of low birthweight (<1000g). Aberrant colonisation with Pseudomonas can also result in NEC, bringing all of the same symptoms and issues I’ve already described.
While Pseudomonas is part of the normal gastrointestinal (GI) flora, it has been known to cause GI infection which can result in fever, skin vesicles, abdominal distention, colonic perforation, necrotising enterocolitis, and anal ulcers. Case fatality rates are as high as 35-50% for Pseudomonas-infected neonates. Endotracheal tube (ETT) colonisation was a significant risk factor for developing bacteraemia, with the fatality rate rising as high as 80% for individuals found to have bacteraemia - a sepsis or blood stream infection. ETT colonisation can persist even after NICU staff institute cleaning and control measures.
In one outbreak reported by french clinicians (Gras-Le Guen et al, 2003), seven very low birthweight neonates became infected with Pseudomonas and four were diagnosed with fulminant septicaemia. While three of the neonates with septicaemia died, two had succumbed to the infection within only hours of symptom onset - so Pseudomonas infection can cause the seemingly healthy looking neonate to ‘crash’ and die in only a very short time. That is the reason we refer to it as ‘a crash’. The fourth died from multiorgan failure six weeks later.
Note the year of publication on the medical journal article above - 2023. Unlike the evidence presented in the Lucy Letby trial, the sudden ‘crashing’ of a neonate is not a new or rare phenomena and is still something we often cannot explain. Research is still ongoing and articles are being published every month looking for explanations and ways to treat the crashed infant.
Another study reported Pseudomonas aeruginosa caused neonatal infective endocarditis (Ooka, 2019). Infection can develop from the respiratory tract in ventilated neonates resulting in ventilatory status deterioration and periods of low oxygen saturation (desats). Some infants will also present with otitis media and discharge from the ears, pneumonia and urinary tract infection (UTI).
Acinetobacter is a nonfermentive gram negative coccobacillus that is ubiquitous in all soils and fresh water, and is regularly found in the hospital environment. The skin of at least 25% of all non-hospitalised individuals is colonised with Acinetobacter, and up to 7% of those also have pharyngeal colonisation. Several studies have identified Acinetobacter species in HWW, both in hospital pipes and as a biofilm on pipe surfaces, sinks and faucets, and theorised that the presence of antibiotics also present in HWW may have led the bacteria to develop antibiotic resistance. There have been several outbreaks of Acinetobacter in UK hospitals, including in neonatal units. Many incidents of infection or outbreak may not be reported in the case literature because authors are more likely to publish cases of success (in defeating the bacteria) than failure (where the infected die). Cases reported in the literature may not be representative of what could be observed in the NICU because it has been suggested that clinicians, especially those who are non-academic, may not have the opportunity to report unusual infections or outbreaks. Acinetobacter can survive on inert surfaces and colonise human skin for extended periods. Some species of Acinetobacter produce verotoxins (Shiga toxin). 89% of Acinetobacter outbreaks in children in hospitals occur in the NICU. Neonates are particularly at risk of unexplained infection and death from this pathogen.
Infection with Acinetobacter was first described in 1951. By 1995, Acinetobacter already accounted for up to 3% of all nosocomial infections. More recent studies have isolated Acinetobacter in 6.9% of hospital-acquired cases of pneumonia, 2.4% of post-admission bloodstream infections (septicaemia), and 1.6% of cases of post-admission urinary tract infection (UTI). Diagnosis of Acinetobacter infection in the past has been unreliable, due to laboratory staff either being unfamiliar with the organism or their assumption that these otherwise endogenous flora were contaminates in the sample.
Any breach of the skin such as intravenous or umbilical catheterisation could result in Acinetobacter infection that could travel around the body and even onto the heart valves. While a rash may not always be seen in the neonate, Acinetobacter infection has been seen to cause a diffuse maculopapular rash that spontaneously appears and fades across the patient’s trunk, arms and legs, or even the palms and soles of the feet. Neonates infected with this pathogen are more likely to be premature. Between 20-57% of patients with Acinetobacter infection may present with enlargement, abscesses and infarction of the spleen, and some patients may also have swelling of the liver. Infected patients have been reported with visceral embolisation partially or completely blocking blood flow to major organs.
Several studies have looked at the various presentations and symptoms arising from Acinetobacter infection in neonates and small infants, which include meningitis, endocarditis, pneumonia and UTI. Acinetobacter infection can cause neonatal infective endocarditis (where bacteria or other infective agents enter the bloodstream and travel to and damage the heart) and often results in bacteraemia (sepsis) and meningitis in infected neonates. Acinetobacter-caused bacteraemia (bloodstream infection) can be diagnosed where the neonate shows hyper- or hypothermia (temperatures too hot or too cold), and spells of apnoea (reduced or absent breathing) or bradycardia (slow heartbeat). Acinetobacter-caused pneumonia can be present where the neonate produced increased respiratory secretions (often seen as strange mucosal fluids collecting in or around the intubation tube), chest x-ray showed pulmonary infiltrates (mucous in the lungs), apnoea, tachypnoea, wheezing, rhonchi or a cough. Some species of Acinetobacter naturally produce haemolysis, resulting in the gradual destruction of the neonates red blood cells. Such haemolytic disease in a neonate could cause them to appear pale, hypoxic (low oxygen saturation and desats), possibly jaundiced, to have generalised oedema (a type of swelling caused by collections of fluids - known as hydrops fetalis), give them the appearance of a swollen belly, and cause there to be blood in their faecal matter. The Shiga toxin produced by Acinetobacter can also cause thrombotic thrombocytopenic purpura - which can be observed as small red or purple splotches on the skin along with lethargy, a low fever, vomiting, diarrhoea, reduced urinary output and sometimes stroke and seizures.
Neonatal deaths are increased, with case fatality rates as high as 40-66% for Acinetobacter-infected neonates. Even with aggressive surveillance, rapid identification of infection and treatment, neonates can remain colonised with Acinetobacter for several weeks.
There are many potential pathogens that we may come into contact with in hospitals - and many are known to grow, and have become disinfectant and antibiotic resistant, in pipes, hand basins, toilets, showers, floor tiles and other areas exposed to hospital wastewater (HWW). Many of these pathogens can survive cleaning, can grow biofilms even inside clean water pipes, under floors and on hospital equipment and, as we will see in the next article, can colonise even new hospital buildings and persist even after those new facilities are thoroughly disinfected.
In this article I have also described many of the more common signs and symptoms of infection with these pathogens. However, and it should be noted, there are case examples in the literature of these pathogens resulting in what we call a silent infection. That is, an infection with no obvious signs or symptoms (until the patient ‘crashes’). The more astute reader will have noticed that several of the signs and symptoms I have described here are similar to those described for numerous babies in the Lucy Letby case. This is something we will also return to in future articles.
NB: In this article I have sought to provide as many plain language definitions for medical terms as I could, and for the sake of easy reading have omitted to provide the academic references. However, at key points through this journey I will also be releasing academic versions of key posts that will contain much of the scientific evidence, citations, and direct references to case examples. Those of you with questions regarding case references can ask below, but I would encourage you to wait for the academic releases.
The next post in the series can be found here.
Having completed much of the training courses and packages provided in the NHS online on-boarding training systems, I can attest first-hand to this stark omission.