Postural drainage and high flow nasal oxygen therapy in four cats with decompensated cardiogenic pulmonary oedema

Abstract

Case series summary

This case series describes four cats with decompensated congestive heart failure and fulminant cardiogenic pulmonary oedema (CPE) that did not respond to conventional treatment and oxygen therapy, and subsequently developed hypoxaemic respiratory failure. The cats were anaesthetised to enable endotracheal intubation, manually ventilated with 100% oxygen and postural drainage was performed immediately to evacuate pulmonary oedema. Afterwards, the cats were extubated and transitioned to high-flow nasal oxygen (HFNO). HFNO allowed significant improvement in the respiration parameters without causing clinical complications. In three of the cats, the procedure was successful; duration of HFNO ranged between 4 and 44 h, and they were successfully weaned off the HFNO therapy. One cat required re-intubation due to HFNO-response failure and was ultimately euthanased. Another cat was euthanased 5 days later due to the severity of its underlying disease.

Relevance and novel information

This is the first report describing the combined technique of postural drainage and HFNO in cats with decompensated CPE. This combined technique could be a life-saving option for cats that fail to respond to conventional therapies and for which positive pressure ventilation is not an option.

Plain language summary

This case series discusses four cats with severe heart failure and sudden, severe fluid build-up in the lungs (cardiogenic pulmonary oedema) that did not improve with standard treatments and oxygen therapy. These cats developed serious breathing problems due to low oxygen levels. To treat them, the cats were put under anaesthesia to allow for a breathing tube to be inserted, and they were manually ventilated with 100% oxygen. Fluid was then drained from their lungs using a special positioning technique (postural drainage). After this procedure, the cats were moved to high-flow nasal oxygen (HFNO) therapy. HFNO significantly improved their breathing without causing any noticeable side effects. Three of the four cats responded well to this treatment, with HFNO therapy lasting between 4 and 44 h, and they eventually recovered. Unfortunately, one cat did not respond to HFNO, required the breathing tube again, and was ultimately euthanased. Another cat was euthanased 5 days later due to the severity of its underlying disease. This is the first report to describe using both postural drainage and HFNO in cats with severe lung fluid build-up due to heart failure. This combined approach may be a life-saving option for cats that do not respond to traditional treatments and cannot undergo positive pressure ventilation

Keywords

Postural drainage high flow nasal oxygen hypoxaemia respiratory distress oxygen therapy

Introduction

Cardiogenic pulmonary oedema (CPE) is a leading cause of cats with respiratory distress being presented to the emergency service.¹ Minimising stress, sedation, oxygen supplementation (eg, oxygen cage) and diuresis induction represents the mainstay in the management of CPE.²

In cases of decompensated CPE and life-threatening respiratory distress, endotracheal intubation (ETI) and manual positive pressure ventilation (PPV) may be necessary to improve oxygen delivery to body tissues and stabilise the patient. Additionally, postural drainage may be needed to remove oedema fluid from the lungs and prevent pulmonary drowning. After intubation and temporary manual ventilation, patients require temporary oxygen therapy with a fraction of inspired oxygen (FiO₂) between 60% and 100%. These high FiO₂ concentrations can be achieved using mechanical PPV, which has been successfully used in dogs and cats suffering from pulmonary oedema secondary to congestive heart failure.³ One disadvantage of PPV is that it is labour-intensive and costly, which may limit its availability and lead to refusal by owners due to financial constraints. High flow nasal oxygen (HFNO) is a system that delivers high flows of humidified, heated air combined with oxygen, allowing for a FiO₂ range between 21% and 100%.⁴ The benefits of HFNO in humans have included improved patient comfort, decreased work of breathing and better oxygenation compared with conventional oxygen therapy.⁵ Limited literature exists on HFNO in cats; there is one case report on a cat with cardiogenic pulmonary oedema and a case series including seven cats with respiratory failure.^6,7

This case series describes four cats presented with fulminant CPE due to decompensated congestive heart failure, in which a specifically designed escalation protocol was applied. This protocol was applied in cats unresponsive to conventional therapy (conventional oxygen therapy, sedation, diuretics) and that were at risk of imminent respiratory failure.

The use of clinical data for research was permitted by the owners as part of the hospital admission procedure.

Case series description

Signalment, clinical characteristics, treatment protocol and outcomes in the four described cats are presented in Table 1. Upon presentation (cases 1–3) or prior the start of the protocol (case 4), respectively, all cats exhibited severe respiratory distress characterised by a respiratory rate between 60 and 80 breaths per minute and at least one of the following: marked respiratory effort with massive chest movements, open-mouth breathing and nasal flaring. Bilateral pulmonary crackles were noted on auscultation in all cats. Cardiovascular assessment revealed a heart rate between 190 and 240 beats per minute and impaired perfusion (eg, pale mucous membranes, prolonged capillary refill time). While none of the cats exhibited a gallop rhythm, one cat (case 4) had a heart murmur. This could also be attributed to concurrent anaemia with a haematocrit of 15% in that cat. Point-of-care ultrasound findings included massive bilateral B-lines, absent pleural effusion, a subjectively thickened left ventricular wall and a subjectively enlarged left atrium:aorta ratio in all cats. These findings led to a strong suspicion of decompensated hypertrophic cardiomyopathy and CPE in all cats.

Table 1

Demographics, clinical characteristics, treatment and outcomes in cats with cardiogenic pulmonary oedema undergoing high flow nasal oxygen therapy (HFNO)

	Case 1	Case 2	Case 3	Case 4
Signalment	Siamese, female spayed, 3 years old, 4.0 kg	Domestic shorthair, male castrated, 10 years old, 7.3 kg	Scottish Straight, female entire, 1 year old, 4.5 kg	Domestic shorthair, female spayed, 8 years old, 4.4 kg
Short history	Sterilised 2 weeks before; intermittent inappetence, lethargy; laboured breathing for 1 day	Lethargy and laboured breathing for 1–2 days	Glucocorticoids for gingivitis 9 days earlier; anorexia, laboured breathing for 1 day	Hospitalised and under treatment with glucocorticoids for anaemia; laboured breathing within hours
Admission/prior HFNO therapy
Mucous membrane colour	Grey–pink	Pale–pink	Pink	Pale–pink
Respiratory rate (bpm)	80	88	80	72
Heart rate (bpm)	200	190	240	220
Cardiac auscultation	No gallop, no murmur	No gallop, no murmur	No gallop, no murmur	No gallop, murmur
Body temperature (ºC)	NA	36.6	36.2	37.0
Dyspnoea score/crackles	4/+++	4/+++	4/+++	4/+++
Total furosemide pre-protocol	8 mg/kg IM over 4 h	4 mg/kg IM	4 mg/kg IM	8 mg/kg IV over 5 h
Duration until start of protocol (h)	5 h	0.5 h	0.5 h	3 h
Anaesthesia for ETI	Butorphanol 0.2 mg/kg IM Midazolam 0.5 mg/kg IM Alphaxalon 1 mg/kg IM	Butorphanol 0.1 mg/kg IM Midazolam 0.3 mg/kg IM Alphaxalon 1 mg/kg IM	Butorphanol 0.3 mg/kg IV Alphaxalon 1 mg/kg IV, to effect	Butorphanol 0.2 mg/kg IV Alphaxalon 1 mg/kg IV, to effect
Postural drainage	3×	3×	3×	2×
After postural drainage:
Dyspnoea score/crackles	3/++	3/+	3/++	2/++
Respiratory rate (bpm)	60	36	60	40
PvCO₂ (mmHg)	73.0	78.0	69.3	35.0
Initial HFNO settings:
Flow (l/min)/FiO₂ (%)/T (°C)	0.5/100/37	1/100/37	1/100/38	1/100/38
Sedation for HFNO	Butorphanol CRI 0.05–0.1 mg/kg/h Midazolam CRI 0.1–0.2 mg/kg/h Propofol CRI 1–3 mg/kg/h	Butorphanol CRI 0.2 mg/kg/h	Butorphanol CRI 0.3 mg/kg/h Midazolam CRI 0.1–0.2 mg/kg/h	Butorphanol CRI 0.05–0.1 mg/kg/h Alphaxalon CRI 4–6 mg/kg/h
SpO₂ increase*	86% (96–100)	85% (95–99)	82% (95–96)	NA (94%)
Total hours on HFNO	44 h	4 h	1 h	12 h
Time until weaning start	24 h	2 h	0	8 h
Diagnosis	HCM phenotype, probable TMT†	HCM phenotype†	Suspected HCM phenotype; gingivitis	IMHA and feline hemotrophic mycoplasmosis; severe hypotension; HCM phenotype†
Response and outcome	Responder; discharge	Responder; discharge	Non-responder: euthanasia (owners declined PPV)	Responder; euthanasia due to underlying disease 5 days later
Long-term outcome	Not known	Euthanasia after 33 weeks	NA	NA

^*Initial value on admission (range after treatment)

^†Diagnosis by a board-certified cardiologist based on echocardiography; dyspnoea score: 0, none; 1, mild; 2, moderate; 3, severe; 4, life-threatening; pulmonary crackles severity: + to +++, mild, moderate, severe

CRI = constant rate infusion; DSH = domestic shorthair; ETI = endotracheal intubation; bpm = either beats (if heart rate) or breaths (if respirators rate) per minute; HCM = hypertrophic cardiomyopathy; IMHA = immune-mediated haemolytic anaemia; NA = not applicable; SpO₂ = haemoglobin oxygen saturation; TMT = transient myocardial thickening

Initial treatment included minimal handling, placement in a climatised oxygen cage set to 60% FiO₂ (Intensovet) and administration of furosemide (Dimazon; MSD Animal Health) (2–4 mg/kg) and butorphanol (Alvegesic 1%; Virbac) (0.2–0.3 mg/kg) either intramuscularly (IM) in cases 1, 2 and 3 or intravenously (IV) in case 4. Additionally, an intravenous catheter was placed in case 3 at this time. As the cats did not respond to this therapy within 15–30 mins (cases 2 and 3) or deteriorated again after initial improvement (cases 1 and 4), the escalation protocol for CPE was applied (Box 1). To enable ETI, anaesthesia was induced with a combination of butorphanol (0.2–0.3 mg/kg), alfaxalone (Alphaxan; Graeub) (1–2 mg/kg and to effect), ± midazolam (Midazolam; Sintetica) (0.2 mg/kg) administered IM or IV. About 7–10 mins after IM and 1–2 mins after intravenous injection, each cat could be taken out of the oxygen cage stress-free. Oxygen was supplemented via a non-occluding mask and a peripheral venous catheter was inserted in cases 1 and 2. As anaesthesia deepened to a level that allowed for urgent yet controlled intubation (either through the natural progression of intramuscular anaesthesia or by administering intravenous alfaxalone to effect), ETI was performed, and the tube cuffed and secured in place. The endotracheal tube (ETT) size, adjusted to each cat’s size, ranged between 4.0 mm (cases 1, 3 and 4) and 4.5 mm (case 2). During intubation, no topical laryngeal analgesia was needed. The cats were ventilated with an Ambu bag (Ambu SPUR II; infant, maximum 150 ml volume; Ambu) and 100% oxygen. Large volumes of oedema fluid were drained from the tube after ETI. Each cat was disconnected from the Ambu bag, held gently in a head-down position and had its chest gently percussed to facilitate postural drainage (Figures 1–2). After 3–4 s, the cat was returned to a sternal position, reconnected to the Ambu bag and manually ventilated with 100% oxygen. This procedure was repeated as needed, based on the amount of oedema fluid draining from the tube – twice in cases 1, 2 and 3, and once in case 4. In between, oedema fluid was carefully suctioned using 6 Fr sterile suction tubes. In case 2, the fluid was redder during the third attempt than initially. Following the postural drainage, significantly fewer crackles were audible on thoracic auscultation, and respiratory pattern and rate improved in all cats. Pulse oximetry revealed increasing haemoglobin oxygen saturation (SpO₂), from 82–86% at the beginning to 95–98% at the end of the procedure. A single-prong infant nasal canula (Solo 1300 High Velocity Nasal Cannula; Vapotherm) was placed under anaesthesia without topical nasal analgesia (Figure 2), sutured bilaterally in the cheek region and connected to the high flow oxygen device (Vapotherm Precision Flow HI-VNI; Vapotherm). The FiO₂ was set at 100%, the flow rate at 1 l/kg/min (except in case 1) and the gas temperature between 37 and 38°C. Cats were sedated primarily with butorphanol constant rate infusion (CRI), with midazolam and alfaxalone CRI administered as needed. Cases 1, 2 and 3 had marked hypercapnia and respiratory acidosis in venous blood gas analysis prior to the start of HFNO.

Box 1

Escalation protocol for cardiogenic pulmonary oedema using postural drainage and high flow nasal oxygen (HFNO)

1. Sedation/anaesthesia and intubation:

• Use a combination of butorphanol (0.2–0.3 mg/kg), midazolam (0.2 mg/kg) and alfaxalone (1–2 mg/kg) IM/IV for sedation

• Consider rapid placement of a peripheral venous catheter

• Once the patient is sufficiently anaesthetised, perform endotracheal intubation and initiate manual ventilation using an Ambu bag with 100% FiO₂

2. Postural drainage:

• Position the intubated cat head-down in an almost vertical position and provide gentle chest percussion to allow oedema fluid to drain through the ETT

• Perform this procedure for 3–4 s, then return the cat to a sternal position and immediately ventilate with 100% oxygen

• Carefully attempt suctioning of oedema fluid through the ETT with a 5–6 Fr tube

• If more fluid is draining from the ETT, repeat the procedure as long as required

3. Initiation of HFNO:

• Achieve sedation using a CRI of butorphanol (0.1–0.3 mg/kg/h). Add midazolam CRI (0.1–0.3 mg/kg/h) and alphaxalon (5–10 mg/kg/h) if necessary and adjust the sedation protocol accordingly. CRIs are mixed in D5W and must be administered at the lowest possible hourly volume (eg, 0.1 ml/kg/h)

• Apply topical lidocaine (2%, maximum 0.05 ml/kg) as nasal drops before placement. Position and secure single-prong nasal canula. If you place double canula, ensure the canula does not exceed 50–70% of the nares’ diameter to allow adequate exhalation

• Initial settings for HFNO: FiO₂ 100%, temperature 36–38°C and flow 1–2 l/kg/min

• Titrate the HFNO device to maintain SpO₂ 94–97%

• Monitor heart rate, temperature, respiratory rate, respiratory effort (chest movement, intercostal retraction and nasal flaring), SpO₂ and partial pressure of venous CO₂. Adjust and document HFNO device settings as needed

4. Weaning of HFNO:

• Ensure the SpO₂ is 94–97% and there is improved work of breathing on stable HFNO-settings for at least 2 h before beginning to wean

• Begin by reducing FiO₂ by 5–10% every 1–2 h until it reaches 40%. Adjust faster if tolerated

• Once FiO₂ is at 40%, start weaning the flow. Decrease the flow by 10–20% every 1–2 h, or faster if tolerated, until reaching a flow of 0.2 l/kg/min

• Continuously monitor the patient’s heart rate, temperature, respiratory rate, respiratory effort and SpO₂ throughout the weaning process, making adjustments as necessary based on the patient’s response

CRI = constant rate infusion; ETT = endotracheal tube; FiO₂ = fraction of inspired oxygen; IM = intramuscular; IV = intravenous; SpO₂ = haemoglobin oxygen saturation

Figure 1

Postural drainage in cats with cardiogenic pulmonary oedema. Following endotracheal intubation and mechanical ventilation with 100% oxygen using an Ambu bag, the patient is disconnected from the Ambu bag (a), gently held in a head-down position and has its chest gently percussed to facilitate drainage (b). After 3–4 s, the cat is returned to a sternal position, reconnected to the Ambu bag and manually ventilated with 100% oxygen (c). If necessary, careful suctioning of oedema fluid through the endotracheal tube is performed (d)

Figure 2

Case 2 was fitted with a single-prong infant nasal canula (right nostril) sutured bilaterally in the cheek region

Case 1 had difficulty accepting the nasal canula (sneezing and face rubbing despite butorphanol and midazolam CRI), resulting in the flow being reduced to 0.5 l/kg/min and adaptation of sedation (propofol CRI was added as not enough alphaxalon was available at that day) (Propofol MCT; Fresenius Kabi). Owing to the increased depth of sedation in case 1, intermittent hypercapnia persisted until propofol was stopped (after 24 h) and sedation reduced. Notably, this cat received HFNO for the longest duration (44 h) and weaning of FiO₂ was not possible until after 24 h. Owing to the long sedation, the cat was not able to drink and, after 20 h, a low volume fluid therapy was started (0.5 ml/kg/h) to avoid hypoperfusion and kidney injury (5% dextrose in 0.9% NaCl, 2:1; Fresenius Kabi). Case 2 improved the best after postural drainage and HFNO-initiation and was sedated with butorphanol CRI alone. After the initial episode and hypertrophic cardiomyopathy (HCM) diagnosis, the cat had two more CPE episodes, treated successfully without HFNO. It was humanely euthanased due to a fourth CPE episode 33 weeks after initial presentation. Case 3 deteriorated after short improvement and required reintubation and manual ventilation. As the owners declined PPV, the cat was finally euthanased at the day of presentation. Case 4 was initially hospitalised for treatment of immune-mediated haemolytic anaemia and feline hemotrophic mycoplasmosis. Five days after successful stabilisation of decompensated CPE, the cat experienced clinical deterioration necessitating vasopressor therapy and further blood transfusions. The owner elected euthanasia due to financial constraints.

All cats received furosemide 1–2 mg/kg q12h or q8h, adjusted to their respiratory pattern, pimobendane (Vetmedin; Boeringer Ingelheim) 0.25 mg/kg q12h (cases 1, 2 and 4), clopidogrel (Clopidogrel; Mepha) 18.75 mg/cat q24h (cases 1 and 2) and unfractionated heparin (Liquemin; Drossapharm) 100 U/kg q8h SC (case 1). Once SpO₂ was between 94% and 97% and work of breathing improved on stable HFNO settings for at least 2 h, the weaning process was started. The time on HFNO was between 4 h and 44 h and weaning was started after 2–24 h. In case 4, weaning was started by reducing the flow (instead of FiO₂), as the cat did not accept the nasal canula anymore with the level of sedation. After successful weaning the cats were transferred to an oxygen cage with 40–50% FiO₂.

Discussion

In this case series, we applied an escalation protocol for CPE in patients that were unresponsive to conventional therapy and were at risk of respiratory failure. In 3/4 cats, the protocol was successful with significant improvement of respiratory rate and work, and oxygenation.

The first step of this protocol is gentle and controlled anaesthesia to enable the intubation and manual ventilation of the patient. Anaesthesia itself is a possible risk factor in these patients, as it can lead to cardiopulmonary arrest. Further, manipulation of the larynx during ETI may lead to laryngospasm and apnoea in cats.^8,9 Nonetheless, we have had a good experience with the described anaesthesia protocol. ETI during the procedure offers several benefits: a safe airway is established over which PPV can be applied with 100% oxygen; the ETT channels fluid out of the mouth, preventing it from dispersing widely, pooling or getting trapped in the oropharyngeal pockets, which could lead to potential aspiration; lastly more distal areas of the trachea (eg, main bronchus) can be suctioned.

Postural drainage is a technique in people where the patient is positioned in different positions to best use gravity to assist in clearing bronchopulmonary secretions from the tracheobronchial tree.¹⁰ It is used, for example, in acute bronchitis in paediatric patients.¹¹ In the present case series, a similar technique was used to drain oedema fluid from the alveoli and airways, by holding the intubated cat carefully in a head-down position and performing gentle chest percussions. In this way, a large amount of oedema fluid can be quickly drained, which can help improve respiratory function and gas exchange. To the best of the authors’ knowledge, there is no peer-reviewed literature addressing postural drainage in cats with CPE, despite its likely regular use in severe feline CPE cases. In forums and websites occasionally, experiential reports can be found. It is also described as the ‘tipping’, ‘teapot’ or ‘tube and dump’ technique. Sometimes it is suggested to also apply pressure to the thorax to expel the oedema fluid. In the present case series, we did not compress the chest and instead performed mild percussion, with the aim of avoiding atelectasis. As reported here, the procedure was performed up to three times for 3–4 s, as repeatedly fluid appeared in the proximal end of the ETT. The procedure must be kept brief, as manual ventilation and oxygen supplementation does not occur during postural drainage, leading to hypoxaemia. Postural drainage in CPE may be associated with adverse effects. In case 2, the drained oedema fluid turned redder, probably reflecting vessel rupture and mild bleeding. Further, head-down positioning can lead to gastroesophageal reflux and aspiration (not observed in the present case series) and it can lead to increased intracranial pressure.

HFNO provides predictable oxygenation, oropharyngeal dead space washout, discrete continuous positive airway pressure (CPAP) (depending on the flow), less inspiratory effort and improved lung volume and compliance.^12
–14 The set-up of the device takes 5–10 mins, and temperature, FiO₂ and flow (l/min) can be adjusted according to the patient’s needs, up to 40 or 60 l/min, depending on the device. In dogs with acute hypoxaemic respiratory failure, HFNO was found to improve oxygenation, respiratory rate and decreased the work of breathing relative to conventional oxygen therapies.^15,16 Described adverse effects and complications in dogs are aerophagia, nasal canula discomfort and subsequent need for sedation, barotrauma and hypercapnia.^13,17

Recently, Pouzot-Nevoret et al⁶ described the successful use of HFNO in a cat with CPE and respiratory distress. The cat was anaesthetised with butorphanol, midazolam and propofol for nasal canula placement and mildly sedated with intermittent butorphanol (0.2 mg/kg IV q4h) during 16 h HFNO therapy. Further, a recent case series was published including seven cats with respiratory failure of various origins.⁷ All cats in these case series tolerated HFNO well without any complications. Two cats accepted nasal canula placement without sedation, and three required no sedation throughout the HFNO therapy. Since, in the present case series, all cats were anaesthetised and intubated, nasal canula placement and fixation was performed under anaesthesia and without topical nasal analgesia (such as 2% lidocaine). The sensitivity of the nasal area complicates secure fixation and high flow rates in an awake patient. In the reported cases here, during HFNO therapy, only case 2 was sedated with a single drug (butorphanol CRI), while all the others required a combination of at least two drugs. In case 1, due to intolerance of the nasal canula despite sedation, the flow rate needed to be limited to 0.5 l /kg/min instead of the recommended minimum of 1 l /kg/min. This cat required the longest duration on HFNO. We hypothesise that a higher flow rate may have improved oxygenation in this cat, based on the effects described above, and consequently led to a shorter duration of HFNO. In addition or instead of using sedation or general anaesthesia, a topical intranasal application of 2% lidocaine can also be considered and is minimally invasive;¹⁸ however, it is potentially stressful and must be repeated regularly at short intervals. In the described cat (case 1), any manipulation of the nasal area (including topical lidocaine) elicited a defensive reaction, leading to opt for deeper sedation and lowering the flow rate.

In all cats, a single-prong nasal canula was used. These present limitations in achieving CPAP: HFNO with a single prong leaves one nostril open, preventing the establishment of the required pressure. Nevertheless, the high flow from the nasal canula offers resistance against expiratory flow and increases airway pressure, which improves oxygenation and reduces the work of breathing. Small double nasal prongs are available; however, these are often too narrow for feline nasal anatomy and may not fit securely. In a study of newborn piglets with induced lung injury treated with HFNO, both ventilation (CO₂ elimination) and oxygenation improved in a flow-dependent manner, regardless of whether single or double prong canulas were used.¹⁹

Different weaning recommendations for HFNO are available in both the human and veterinary literature, with a common approach being to first reduce the FiO₂ (eg, to 50% FiO₂) before decreasing the flow rate.12,20 –22 The rationale behind this strategy is to increase airway pressure, reduce the work of breathing and limit the risk of oxygen intoxication. Further, the ratio of SpO₂/FiO₂ to respiratory rate (ROX index) was found to have a high accuracy for predicting successful weaning off HFNO treatment in patients with COVID-19 pneumonia.²³ These findings suggest that the ROX index could potentially be used in veterinary patients to guide the weaning process. No randomised controlled studies on this weaning strategy are yet available for small animals.

Conclusions

The technique described here is an option for the management of cats with decompensated CPE and hypoxaemic failure. A standardised protocol in these situations ensures quick, effective and consistent care, optimising efficiency and outcome.

Footnotes

Accepted: 6 November 2024

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

The work described in this manuscript involved the use of non-experimental (owned or unowned) animals. Established internationally recognised high standards (‘best practice’) of veterinary clinical care for the individual patient were always followed and/or this work involved the use of cadavers. Ethical approval from a committee was therefore not specifically required for publication in JFMS. Although not required, where ethical approval was still obtained, it is stated in the manuscript.

Informed consent

Informed consent (verbal or written) was obtained from the owner or legal custodian of all animal(s) described in this work (experimental or non-experimental animals, including cadavers, tissues and samples) for all procedure(s) undertaken (prospective or retrospective studies). For any animals or people individually identifiable within this publication, informed consent (verbal or written) for their use in the publication was obtained from the people involved.

ORCID iD

Katja-Nicole Adamik

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